Sarcomerogenesis,the addition of serial sarcomeres in skeletal muscle myofibrils and fibres,is a natural occurrence during growth and maturation of animals,including humans.However,the detailed mechanisms that allow f...Sarcomerogenesis,the addition of serial sarcomeres in skeletal muscle myofibrils and fibres,is a natural occurrence during growth and maturation of animals,including humans.However,the detailed mechanisms that allow for sarcomerogenesis are not fully understood.In some diseases,such as cerebral palsy in children,sarcomerogenesis appears to be inhibited or at least reduced,1,2 often causing severe restrictions in muscle and joint function.展开更多
Skeletal muscle dysfunction is a common extrapulmonary comorbidity of chronic obstructive pulmonary disease(COPD) and is associated with decreased quality-of-life and survival in patients. The autophagy lysosome pathw...Skeletal muscle dysfunction is a common extrapulmonary comorbidity of chronic obstructive pulmonary disease(COPD) and is associated with decreased quality-of-life and survival in patients. The autophagy lysosome pathway is one of the proteolytic systems that significantly affect skeletal muscle structure and function. Intriguingly, both promoting and inhibiting autophagy have been observed to improve COPD skeletal muscle dysfunction, yet the mechanism is unclear. This paper first reviewed the effects of macroautophagy and mitophagy on the structure and function of skeletal muscle in COPD, and then explored the mechanism of autophagy mediating the dysfunction of skeletal muscle in COPD. The results showed that macroautophagy-and mitophagy-related proteins were significantly increased in COPD skeletal muscle. Promoting macroautophagy in COPD improves myogenesis and replication capacity of muscle satellite cells, while inhibiting macroautophagy in COPD myotubes increases their diameters. Mitophagy helps to maintain mitochondrial homeostasis by removing impaired mitochondria in COPD. Autophagy is a promising target for improving COPD skeletal muscle dysfunction, and further research should be conducted to elucidate the specific mechanisms by which autophagy mediates COPD skeletal muscle dysfunction, with the aim of enhancing our understanding in this field.展开更多
BACKGROUND Improving our understanding of whether increased dietary intake ofω-3 polyunsaturated fatty acids(PUFAs)is beneficial for increasing skeletal muscle mass in patients with metabolic dysfunction-associated f...BACKGROUND Improving our understanding of whether increased dietary intake ofω-3 polyunsaturated fatty acids(PUFAs)is beneficial for increasing skeletal muscle mass in patients with metabolic dysfunction-associated fatty liver disease(MAFLD)could provide an important clinical evidence base for the development of relevant nutritional guidelines.AIM To investigate the effect of total dietaryω-3 PUFAs and their subtypes on skeletal muscle mass in MAFLD.METHODS This cross-sectional study involved 2316 participants from four National Health and Nutrition Examination Survey cycles between 2011 and 2018.Dietary intake ofω-3 PUFAs was collected through 24-hour dietary recall interviews.Appendicular skeletal muscle mass index(ASMI)was calculated by dividing ASM in kilograms by height squared.RESULTS The multiple linear regression model showed significant relationships for dietary intake of totalω-3 PUFAs with higher ASMI(β:0.06,95%CI:0.01-0.11)in MAFLD patients.Dietary a-linolenic acid(ALA)(β:0.06,95%CI:0.01-0.12),docosapentaenoic acid(β:1.28,95%CI:0.01-2.54),and docosahexaenoic acid(DHA)(β:0.19,95%CI:0.01-0.37)were significantly associated with higher ASMI,while intake of stearidonic acid and eicosapentaenoic acid did not improve ASMI.In patients with high probability of liver fibrosis,dietary intake of ALA was associated with higher ASMI(β:0.11,95%CI:0.03-0.18).Stratified analysis found that DHA was associated with higher ASMI in patients with obesity and higher metabolic risk.CONCLUSION Increasing dietary intake ofω-3 PUFAs improved skeletal muscle health in patients with MAFLD.Patient with obesity and higher metabolic risk were more likely to benefit from intake of DHA.展开更多
1.Exercise enhances muscle function and insulin sensitivity Skeletal muscle plays a fundamental role in not only locomotion,but also systemic metabolism.In people with type 2 diabetes,skeletal muscle is a major site o...1.Exercise enhances muscle function and insulin sensitivity Skeletal muscle plays a fundamental role in not only locomotion,but also systemic metabolism.In people with type 2 diabetes,skeletal muscle is a major site of insulin resistance,with impaired insulin signaling and reduced glucose transport activity contributing to metabolic dysfunction.展开更多
Background While maternal proline(Pro)supplementation has demonstrated efficacy in enhancing placental angiogenesis and farrowing efficiency in swine,its regulatory role in fetal skeletal muscle ontogeny remains undef...Background While maternal proline(Pro)supplementation has demonstrated efficacy in enhancing placental angiogenesis and farrowing efficiency in swine,its regulatory role in fetal skeletal muscle ontogeny remains undefined.This study systematically evaluated the temporal-specific impacts of dietary Pro supplementation during critical phases of fetal myogenesis(encompassing primary myofiber formation and secondary myofiber hyperplasia)on offspring muscle development.A total of 120 sows with similar farrowing schedules were assigned to three groups:CON(basal diet),ST-Pro(0.5%Pro supplementation during secondary myofiber formation period,from d 60 gestation to farrowing),LT-Pro(0.5%Pro supplementation spanning primary and secondary myofiber formation period:from d 20 gestation to farrowing).Results LT-Pro group significantly increased the longissimus dorsi(LD)muscle mass per unit body weight in newborn piglets compared to CON group(P<0.05),while no such effect was observed in the ST-Pro group.Metabolomic profiling revealed elevated Pro,lysine,and tryptophan levels in the LD muscle of LT-Pro group piglets,accompanied by reduced branched-chain amino acids(BCAAs;leucine,isoleucine,and valine)in both serum and muscle(P<0.05).Histological analysis demonstrated a 45.74%increase in myofiber cross-sectional area in the LT-Pro group(P<0.05).At the molecular level,LT-Pro group piglets exhibited upregulated mRNA expression levels of myogenic regulatory genes(MYOD1,MYF6)and the cell cycle accelerator CCND1(P<0.05),coupled with activation of the STAT3 signaling pathway(phosphorylated STAT3 protein increased by 2.53-fold,P<0.01).Furthermore,Pro supplementation enhanced oxidative metabolism,evidenced by elevated mitochondrial biogenesis markers(the mRNA expression levels of PPARGC1A,OPA1,and SQSTM1)and a 61.58%increase in succinate dehydrogenase activity(P<0.05).Notably,LT-Pro group piglets showed a selective shift toward slow-twitch oxidative fibers,with both MyHC1 mRNA and protein expression levels significantly upregulated(P<0.05),while the mRNA expression levels of MyHCIIb showed no significant change.Conclusions This study identified the primary fiber formation period as a critical window.Supplementation with Pro during G20–114 reprogrammed offspring skeletal muscle development through STAT3-CCND1-mediated myoblast proliferation,enhanced mitochondrial bioenergetics,and oxidative fiber specification.However,no such effects were observed during G60–114.These findings propose maternal Pro intervention as a novel strategy to enhance muscle yield and metabolic efficiency in swine production,with potential applications for improving meat quality traits linked to oxidative muscle phenotypes.展开更多
Metabolic dysfunction-associated steatotic liver disease is increasingly understood to be closely linked with skeletal muscle alterations,such as sarcopenia,myoste-atosis,and metabolic dysregulation,which play a key r...Metabolic dysfunction-associated steatotic liver disease is increasingly understood to be closely linked with skeletal muscle alterations,such as sarcopenia,myoste-atosis,and metabolic dysregulation,which play a key role in its pathogenesis and progression.Recent literature,including an article by Isakov,highlights the bidirectional interactions between muscle and liver,underscoring shared mechanisms such as insulin resistance,inflammation,and myokine imbalance.This letter reflects on key findings from the review,noting strengths such as its integration of mechanistic insights,discussion of emerging biomarkers,and emphasis on lifestyle and pharmacological interventions.It also identifies areas for further development,including standardization of diagnostic criteria and more rigorous evaluation of translational data.As muscle health gains promi-nence in metabolic dysfunction-associated steatotic liver disease research,multidisciplinary strategies that target both hepatic and muscular systems may offer more effective avenues for prevention and treatment.展开更多
BACKGROUND Skeletal muscle alterations(SMAs)are being increasingly recognized in patients with metabolic dysfunctionassociated steatotic liver disease(MASLD)and appear to be associated with deleterious outcomes in the...BACKGROUND Skeletal muscle alterations(SMAs)are being increasingly recognized in patients with metabolic dysfunctionassociated steatotic liver disease(MASLD)and appear to be associated with deleterious outcomes in these patients.However,their actual prevalence and pathophysiology remain to be elucidated.AIM To determine the prevalence of SMAs and to assess the significance of circulating myokines as biomarkers in patients with MASLD.METHODS Skeletal muscle strength and muscle mass were measured in a cross-sectional study in a cohort of 62 patients fulfilling MASLD criteria,recruited from the outpatient clinics of a tertiary level hospital.The degree of fibrosis and liver steatosis was studied using abdominal ultrasound and transitional elastography.Anthropometric and metabolic characteristics as well as serum levels of different myokines were also determined in the MASLD cohort.Statistical analysis was performed comparing results according to liver fibrosis and steatosis.RESULTS No significant differences were found in both skeletal muscle strength and skeletal muscle mass in patients with MASLD between different stages of liver fibrosis.Interestingly,serum levels of fibroblast growth factor-21(FGF21)were significantly higher in patients with MASLD with advanced hepatic fibrosis(F3-F4)than in those with lower fibrosis stages(F0-F2)(197.49±198.27 pg/mL vs 95.62±83.67 pg/mL;P=0.049).In addition,patients with MASLD with severe hepatosteatosis(S3)exhibited significantly higher serum levels of irisin(1116.87±1161.86 pg/mL)than those with lower grades(S1-S2)(385.21±375.98 pg/mL;P=0.001).CONCLUSION SMAs were uncommon in the patients with MASLD studied.Higher serum levels of irisin and FGF21 were detected in patients with advanced liver steatosis and fibrosis,respectively,with potential implications as biomarkers.展开更多
Background: Aging-induced cardiac hypertrophy and reduced skeletal muscle strength contribute to increased disease risk and life burden in the elderly. FNDC5 acts as a protective muscle factor in both cardiac and skel...Background: Aging-induced cardiac hypertrophy and reduced skeletal muscle strength contribute to increased disease risk and life burden in the elderly. FNDC5 acts as a protective muscle factor in both cardiac and skeletal muscle. This study aims to examine the relationship between cardiac FNDC5 and aging-related cardiac hypertrophy and decreased skeletal muscle strength. Methods: Male young C57BL/6 mice (5 months old, n = 6) and aged mice (21 months old, n = 6) were utilized in the study and housed in a specific pathogen-free (SPF) environment. Prior to the experiment, grip strength tests were performed on the mice, and heart tissues were collected for morphological analysis, including the assessment of peroxisome proliferator-activated receptor gamma coactivator 1α (PGC-1α) and fibronectin type III-containing structural domain 5 (FNDC5) protein levels. Furthermore, myosin heavy chain II (MyHC II), skeletal muscle-specific transcription factor (MyoD), muscle RING-finger protein-1 (MuRF1), and FNDC5 levels were evaluated in the quadriceps muscle. The correlations between heart weight and FNDC5 expression levels, as well as skeletal muscle indices in the mice, were subsequently analyzed. Result: Aging leads to cardiac hypertrophy and reduced expression of PGC-1α and FNDC5 proteins. Concurrently, there is a decline in the strength of skeletal muscle, along with decreased expression of MyHC II and increased expression of MURF1 and MyoD. Correlation analysis demonstrated strong positive associations between myocardial FNDC5 protein levels and limb grip strength, as well as MyHC II, and strong negative associations with MyoD and MuRF1. Conclusion: There may be a significant association between aging-induced cardiac hypertrophy and decreased skeletal muscle strength, with FNDC5 potentially playing a crucial role as a regulatory molecule facilitating communication between the heart and skeletal muscle.展开更多
Highland barley tea(HBT)is made from roasted barley seeds and is abundant inβ-glucan,amino acids,minerals,phenolics,and other natural active ingredients.These natural compounds found in whole grains have been shown t...Highland barley tea(HBT)is made from roasted barley seeds and is abundant inβ-glucan,amino acids,minerals,phenolics,and other natural active ingredients.These natural compounds found in whole grains have been shown to slow aging and positively affect skeletal muscle function.As a result,studying the effects of HBT on the skeletal muscle health of the elderly population is critical from a scientific and societal standpoint for improving their health status and reducing the medical burden on society.The antioxidant activity and the content of natural active substances were used as indicators to screen the optimal process of HBT brewing.The effects of long-term HBT consumption on aging in mice were investigated by using HBT as a substitute for drinking water in naturally aging mice for a 5-month intervention.Afterward,various factors were measured,such as basic physiological indices,inflammation,plasma metabolites,skeletal muscle function,and exercise capacity,to evaluate the effects of HBT on aging in mice.Long-term consumption of HBT reduced body and spleen weight,increased body weight percentage of skeletal muscle,and reduced plasma inflammation levels in aging mice.Metabolomic results showed increased plasma levels of the mitochondrial marker short-chain acylcarnitine and some amino acids.Additionally,there was a decrease in bile and long-chain acylcarnitine.The level of fibrosis in the gastrocnemius muscle of aging mice was suppressed,and the percentage of typeⅠmuscle fibers was increased,improving the endurance of the mice.Thus,long-term consumption of HBT may reduce body weight and increase skeletal muscle mitochondrial activity and exercise capacity in aging mice by reducing inflammation levels and alleviating mitochondrial damage.展开更多
BACKGROUND Many studies have found that sarcopenia is related to the survival of patients with liver cancer,which may lead to worse prognosis.AIM To investigate the relationship between skeletal muscle mass and progno...BACKGROUND Many studies have found that sarcopenia is related to the survival of patients with liver cancer,which may lead to worse prognosis.AIM To investigate the relationship between skeletal muscle mass and prognosis in patients with liver cancer receiving targeted therapy by meta-analysis.METHODS PubMed,Embase,Cochrane Library,and Web of Science were searched for clinical studies on the relationship between skeletal muscle index(SMI)and the prognosis of patients with liver cancer receiving targeted therapy from inception to March 1,2022.Meta-analysis and sensitivity analysis of the data were performed using Stata 16.0 software.RESULTS A total of 6877 studies were searched,and finally 12 articles with 1715 cases were included.Meta-analysis result of 8 articles showed that compared with non-low SMI group,the overall survival(OS)of patients with liver cancer in the low SMI group was significantly shorter(hazard ratio=1.60,95%confidence interval:1.44-1.77,P=0.000).Meta-analysis result of 4 articles showed that,compared with low SMI group,patients in the nonlow SMI group had longer OS(hazard ratio=0.59,95%confidence interval:0.38-0.91,P=0.018).CONCLUSION Skeletal muscle mass is positively correlated with OS in patients with liver cancer receiving targeted therapy.展开更多
Obesity is associated with skeletal muscle mass loss and physical dysfunction.Krill oil(KO)has been shown to be beneficial in human health.However,the effect of KO on obesity-induced skeletal muscle atrophy is still u...Obesity is associated with skeletal muscle mass loss and physical dysfunction.Krill oil(KO)has been shown to be beneficial in human health.However,the effect of KO on obesity-induced skeletal muscle atrophy is still unclear.In this study,the male C57BL/6J mice were fed a high-fat diet(HFD)for 12 weeks to induce obesity,and then were intragastric administration with 400 mg/kg bw KO for an additional 6 weeks.The results showed that KO treatment reduced body weight,fat accumulation and serum pro-inflammatory cytokines in HFD-induced obese mice.Importantly,KO treatment attenuated skeletal muscle atrophy in HFD-fed mice,as evidenced by preserving skeletal muscle mass,average myofiber cross-sectional area and grip strength.KO administration also mitigated obesity-induced ectopic lipid deposition and inflammatory response in skeletal muscle.Additionally,KO treatment inhibited the transcriptional activities of nuclear factor-κB(NF-κB)p65 and forkhead box O 3a(FoxO3a),and then down-regulated muscle atrophy F-box(MAFbx)and muscle-specific RING finger protein 1(MuRF1)protein levels in skeletal muscle from HFD-fed mice.KO administration also improved obesity-induced impaired muscle protein synthesis via activating PI3K/Akt pathway.Furthermore,KO treatment enhanced muscle mitochondrial biogenesis in HFD-induced obese mice via activating PGC-1αpathway.Collectively,KO might be developed as a potential nutritional supplement for the prevention and treatment of obesity-induced skeletal muscle atrophy.展开更多
Objectives:Skeletal muscle ischemia/reperfusion injury(IRI)occurs as a result of a marked reduction in arterial perfusion to a limb and can lead to tissue death and threaten limb viability.This work assessed the effec...Objectives:Skeletal muscle ischemia/reperfusion injury(IRI)occurs as a result of a marked reduction in arterial perfusion to a limb and can lead to tissue death and threaten limb viability.This work assessed the effects of 20-hydroxyecdysone(20E)on hindlimb skeletal tissue following tourniquet-induced ischemia/reperfusion injury.Methods:Animals were divided into 4 groups—control group(Control),Control+20E(C+20E),mice with IRI(IRI),and mice with IRI+20E(IRI+20E).IRI was modeled by applying a tourniquet to the hind limb for 2 h with reperfusion for 1 h.5 mg/kg of 20E was administered intraperitoneally for 14 days.Afterward,the physical activity of mice,the histological structure of the quadriceps femoris,the expression of genes encoding proteins induced by hypoxia and involved in tissue adaptation to ischemia,and the functional parameters of skeletal muscle mitochondria were assessed.Results:It was shown that IRI of the limbs leads to functional disorders,depression of muscle function,accumulation of malondialdehyde(MDA)in mitochondria,and a decrease in their Ca2+buffering capacity,as well as an increase in the expression of HIF-1α,VGEF-A,PGC1αand PDGF-BB genes associated with adaptation to ischemia.20E reduced the intensity of degenerative processes in skeletal muscles,which was expressed in a decrease in the number of centrally nucleated fibers.Analysis of gene expression levels indicated a high degree of adaptation of animals to IRI.20E reduced the level of MDA in mitochondria,but did not affect the rate of respiration and calcium retention capacity of organelles both in normal conditions and during IRI.Conclusion:20E partially alleviates the skeletal muscle damage caused by IRI and can be used as part of combination therapy.展开更多
The skeletal muscle is the largest organ present in the body and is responsible for mechanical activities like maintaining posture,movement,respiratory function,and support for the health and functioning of other syst...The skeletal muscle is the largest organ present in the body and is responsible for mechanical activities like maintaining posture,movement,respiratory function,and support for the health and functioning of other systems of the body.Skeletal muscle atrophy is a condition characterized by a reduction in muscle size,strength,and activity,which leads to an increased dependency on others for movement,an increased risk of falls,and a reduced quality of life.Various conditions like osteoarthritis,osteoporosis,and fractures are directly associated with increased muscle atrophy.Additionally,numerous risk factors,like aging,malnutrition,physical inactivity,and certain disease conditions,through distinct pathways,negatively affect skeletal muscle health and lead to muscle atrophy.Among various determinants of overall muscle health,the rate of muscle protein synthesis and degradation is an important parameter that eventually alters the fate of overall muscle health.In conditions of excessive skeletal muscle atrophy,including sarcopenia,the rate of muscle protein degradation usually exceeds the rate of protein synthesis.The availability of amino acids in the systemic circulation is a crucial step in muscle protein synthesis.The current review aims to consolidate the existing evidence on amino acids,highlight their mechanisms of action,and assess their roles and effectiveness in enhancing skeletal muscle health.展开更多
Skeletal muscles are essential for locomotion,posture,and metabolic regulation.To understand physiological processes,exercise adaptation,and muscle-related disorders,it is critical to understand the molecular pathways...Skeletal muscles are essential for locomotion,posture,and metabolic regulation.To understand physiological processes,exercise adaptation,and muscle-related disorders,it is critical to understand the molecular pathways that underlie skeletal muscle function.The process of muscle contra ction,orchestrated by a complex interplay of molecular events,is at the core of skeletal muscle function.Muscle contraction is initiated by an action potential and neuromuscular transmission requiring a neuromuscular junction.Within muscle fibers,calcium ions play a critical role in mediating the interaction between actin and myosin filaments that generate force.Regulation of calcium release from the sarcoplasmic reticulum plays a key role in excitation-contraction coupling.The development and growth of skeletal muscle are regulated by a network of molecular pathways collectively known as myogenesis.Myogenic regulators coordinate the diffe rentiation of myoblasts into mature muscle fibers.Signaling pathways regulate muscle protein synthesis and hypertrophy in response to mechanical stimuli and nutrient availability.Seve ral muscle-related diseases,including congenital myasthenic disorders,sarcopenia,muscular dystrophies,and metabolic myopathies,are underpinned by dys regulated molecular pathways in skeletal muscle.Therapeutic interventions aimed at preserving muscle mass and function,enhancing regeneration,and improving metabolic health hold promise by targeting specific molecular pathways.Other molecular signaling pathways in skeletal muscle include the canonical Wnt signaling pathway,a critical regulator of myogenesis,muscle regeneration,and metabolic function,and the Hippo signaling pathway.In recent years,more details have been uncovered about the role of these two pathways during myogenesis and in developing and adult skeletal muscle fibers,and at the neuromuscular junction.In fact,research in the last few years now suggests that these two signaling pathways are interconnected and that they jointly control physiological and pathophysiological processes in muscle fibers.In this review,we will summarize and discuss the data on these two pathways,focusing on their concerted action next to their contribution to skeletal muscle biology.However,an in-depth discussion of the noncanonical Wnt pathway,the fibro/a dipogenic precursors,or the mechanosensory aspects of these pathways is not the focus of this review.展开更多
BACKGROUND Fibro-adipogenic progenitors(FAPs)are a group of mesenchymal stem cells that cause fibro-fatty degeneration in skeletal muscle in various chronic disease mode-ls.FAPs also play a role in preventing muscle d...BACKGROUND Fibro-adipogenic progenitors(FAPs)are a group of mesenchymal stem cells that cause fibro-fatty degeneration in skeletal muscle in various chronic disease mode-ls.FAPs also play a role in preventing muscle degeneration at acute stages during disease progression.However,few studies have reported the changes in and function of FAPs in the acute phase after tendon rupture.AIM To clarify the changes in the number of FAPs and their impact on skeletal muscle soon after tendon rupture to facilitate future studies targeting FAPs to treat muscle degeneration.METHODS We utilized Pdgfra-H2B::eGFP mice to trace and quantify FAPs in a tibialis anterior tenotomy(TAT)model at 0 and 3 days,1 week,2 weeks,3 weeks,4 weeks,5 weeks,and 6 weeks post-injury,and the results were further validated using fluorescence-activated cell sorting analysis with C57BL/6 mice at the same post-injury timepoints.We subsequently used PdgfraCreERT::RosaDTA mice,and evaluated the severity of post-TAT skeletal muscle degeneration with or without FAP-depletion.RESULTS The number of FAPs peaked at 1 week post-TAT before gradually declining to a level comparable to that pre-TAT.The change in the number of FAPs was potentially temporally correlated with the progression of skeletal muscle degeneration after TAT.FAP-depletion led to more severe degeneration early after TAT,indicating that FAPs potentially alleviate muscle degeneration after tendon rupture in the early post-injury phase.CONCLUSION FAPs potentially alleviate the degeneration of skeletal muscle in the acute stage after tendon rupture.展开更多
BACKGROUND Metastasis of renal cell carcinoma(RCC)to the skeletal muscle and small bowel is an exceedingly rare occurrence.Both of these sites are unusual sites for RCC to metastasize to and to occur simultaneously is...BACKGROUND Metastasis of renal cell carcinoma(RCC)to the skeletal muscle and small bowel is an exceedingly rare occurrence.Both of these sites are unusual sites for RCC to metastasize to and to occur simultaneously is even less common.CASE SUMMARY A 58-year-old male with known history of RCC presented with a recurrence that was diagnosed through imaging and biopsies.Mucosa abnormalities of small bowel noted during endoscopy were biopsied as well as lesion in the psoas muscle that was noted.CONCLUSION This case report emphasizes that RCC can not only recur but can do so even decades later and present as metastatic foci at atypical sites.展开更多
OBJECTIVE:To explore the effect of electroacupuncture on skeletal muscle pain in Parkinson's disease(PD).METHODS:A single-center randomized controlled trial was conducted with sixty patients with Parkinson's d...OBJECTIVE:To explore the effect of electroacupuncture on skeletal muscle pain in Parkinson's disease(PD).METHODS:A single-center randomized controlled trial was conducted with sixty patients with Parkinson's disease with skeletal muscle pain were randomly divided into electroacupuncture group and sham acupuncture control group with 30 patients each.The electric acupuncture group was treated with electric acupuncture,while the control group was treated with Park needle pseudoacupuncture.Both groups were treated 5 times a week for a total of 4 weeks,and both groups completed 20 treatments.King's Parkinson's Pain Scale(KPPS)and visual analog scale(VAS)were used before and after treatment to evaluate the pain degree of patients.Realtime shear wave elastography(SWE)and modified Ashworth score(MAS)were used to evaluate the changes of muscle tone.Parkinson's comprehensive Score Scale(MDS-UPDRS,including UPDRS Ⅱ and UPDRS Ⅲ)was used to evaluate exercise ability.Hamilton Depression Scale(HAMD)score was used to evaluate the emotional changes of patients.Spearman correlation analysis was used to explore the correlation between pain degree and muscle tone,exercise ability and emotion.RESULTS:During the study,one case fell off in the control group,and 30 cases were eventually included in the analysis and treatment group and 29 cases in the control group.After treatment,Young's modulus of biceps and quadriceps and shear wave velocity of biceps were decreased in electroacupuncture group compared with before treatment,while KPPS score,VAS score,UPDRS Ⅱ,UPDRS Ⅲ and modified Ashworth score were decreased,with statistical significance(P<0.05).There was no statistical significance in control group(P>0.05).After treatment,KPPS score,VAS score,UPDRS Ⅱ and UPDRS Ⅲ,MAS,HAMD score,Young's modulus of biceps and shear wave velocity in electroacupuncture group were significantly lower than those in control group(P<0.05).Spearman correlation analysis showed that KPPS score was positively correlated with UPDRS Ⅲ(r=0.414,P<0.05).KPPS score was positively correlated with HAMD score(r=0.576,P<0.01).CONCLUSION:Electroacupuncture therapy can effectively improve skeletal muscle pain in patients with Parkinson's disease,reduce the muscle hardness of patients,improve patients'daily life ability,and improve patients'emotional disorders.The degree of skeletal muscle pain in PD patients is correlated with motor ability and emotional disorders,but there is no significant correlation between the degree of skeletal muscle pain and the muscle tone of PD patients.展开更多
Amyotrophic lateral sclerosis is a fatal multisystemic neurodegenerative disease with motor neurons being a primary target.Although progressive weakness is a hallmark feature of amyotrophic lateral sclerosis,there is ...Amyotrophic lateral sclerosis is a fatal multisystemic neurodegenerative disease with motor neurons being a primary target.Although progressive weakness is a hallmark feature of amyotrophic lateral sclerosis,there is considerable heterogeneity,including clinical presentation,progression,and the underlying triggers for disease initiation.Based on longitudinal studies with families harboring amyotrophic lateral sclerosis-associated gene mutations,it has become apparent that overt disease is preceded by a prodromal phase,possibly in years,where compensatory mechanisms delay symptom onset.Since 85-90%of amyotrophic lateral sclerosis is sporadic,there is a strong need for identifying biomarkers that can detect this prodromal phase as motor neurons have limited capacity for regeneration.Current Food and Drug Administration-approved therapies work by slowing the degenerative process and are most effective early in the disease.Skeletal muscle,including the neuromuscular junction,manifests abnormalities at the earliest stages of the disease,before motor neuron loss,making it a promising source for identifying biomarkers of the prodromal phase.The accessibility of muscle through biopsy provides a lens into the distal motor system at earlier stages and in real time.The advent of“omics”technology has led to the identification of numerous dysregulated molecules in amyotrophic lateral sclerosis muscle,ranging from coding and non-coding RNAs to proteins and metabolites.This technology has opened the door for identifying biomarkers of disease activity and providing insight into disease mechanisms.A major challenge is correlating the myriad of dysregulated molecules with clinical or histological progression and understanding their relevance to presymptomatic phases of disease.There are two major goals of this review.The first is to summarize some of the biomarkers identified in human amyotrophic lateral sclerosis muscle that have a clinicopathological correlation with disease activity,evidence of a similar dysregulation in the SOD1G93A mouse during presymptomatic stages,and evidence of progressive change during disease progression.The second goal is to review the molecular pathways these biomarkers reflect and their potential role in mitigating or promoting disease progression,and as such,their potential as therapeutic targets in amyotrophic lateral sclerosis.展开更多
The“longevity protein”SIRT5 could hold the key to delaying age-related muscle decline.A study led by researchers from the Institute of Zoology(IOZ)of the Chinese Academy of Sciences and Capital Medical University in...The“longevity protein”SIRT5 could hold the key to delaying age-related muscle decline.A study led by researchers from the Institute of Zoology(IOZ)of the Chinese Academy of Sciences and Capital Medical University in Beijing reveals that SIRT5 mitigates skeletal muscle aging by blocking pro-inflammatory pathways.Published in Nature Metabolism on March 14,2025,the work identifies SIRT5’s interaction with protein kinase TBK1 as critical to preserving muscle mass and function.展开更多
Objective:To investigate the effects of acupotomy on skeletal muscle fibrosis and collagen deposition in a rabbit knee osteoarthritis(KOA)model.Methods: Rabbits(n=18)were randomly divided into control,KOA,and KOA+acup...Objective:To investigate the effects of acupotomy on skeletal muscle fibrosis and collagen deposition in a rabbit knee osteoarthritis(KOA)model.Methods: Rabbits(n=18)were randomly divided into control,KOA,and KOA+acupotomy(Apo)groups(n=6).The rabbits in the KOA and Apo groups were modeled using the modified Videman's method for 6 weeks.After modeling,the Apo group was subjected to acupotomy once a week for 3 weeks on the vastus medialis,vastus lateralis,rectus femoris,biceps femoris,and anserine bursa tendons around the knee.The behavior of all animals was recorded,rectus femoris tissue was obtained,and histomorphological changes were observed using Masson staining and transmission electron microscopy.The expression of transforming growth factor-β1(TGF-β1),Smad 3,Smad 7,fibrillar collagen types I(Col-I)and III(Col-III)was detected using Western blot and real-time polymerase chain reaction(RT-PCR).Results: Histological analysis revealed that acupotomy improved the microstructure and reduced the collagen volume fraction of rectus femoris,compared with the KOA group(P=.034).Acupotomy inhibited abnormal collagen deposition by modulating the expression of fibrosis-related proteins and mRNA,thus preventing skeletal muscle fibrosis.Western blot and RT-PCR analysis revealed that in the Apo group,Col-I,and Col-III protein levels were significantly lower than those in the KOA group(both P<.01),same as Col-I and Col-III mRNA levels(P=.0031;P=.0046).Compared with the KOA group,the protein levels of TGF-β1 and Smad 3 were significantly reduced(both P<.01),as were the mRNA levels of TGF-β1 and Smad 3(P=.0007;P=.0011).Conversely,the levels of protein and mRNA of Smad 7 were significantly higher than that in the KOA group(P<.01;P=.0271).Conclusion: Acupotomy could alleviate skeletal muscle fibrosis and delay KOA progress by inhibiting collagen deposition through the TGF-β/Smad pathway in the skeletal muscle of KOA rabbits.展开更多
文摘Sarcomerogenesis,the addition of serial sarcomeres in skeletal muscle myofibrils and fibres,is a natural occurrence during growth and maturation of animals,including humans.However,the detailed mechanisms that allow for sarcomerogenesis are not fully understood.In some diseases,such as cerebral palsy in children,sarcomerogenesis appears to be inhibited or at least reduced,1,2 often causing severe restrictions in muscle and joint function.
基金supported by the National Natural Science Foundation of China(No.82172551)the Health Discipline Leader Project of Shanghai Municipal Health Commission(No.2022XD044),China.
文摘Skeletal muscle dysfunction is a common extrapulmonary comorbidity of chronic obstructive pulmonary disease(COPD) and is associated with decreased quality-of-life and survival in patients. The autophagy lysosome pathway is one of the proteolytic systems that significantly affect skeletal muscle structure and function. Intriguingly, both promoting and inhibiting autophagy have been observed to improve COPD skeletal muscle dysfunction, yet the mechanism is unclear. This paper first reviewed the effects of macroautophagy and mitophagy on the structure and function of skeletal muscle in COPD, and then explored the mechanism of autophagy mediating the dysfunction of skeletal muscle in COPD. The results showed that macroautophagy-and mitophagy-related proteins were significantly increased in COPD skeletal muscle. Promoting macroautophagy in COPD improves myogenesis and replication capacity of muscle satellite cells, while inhibiting macroautophagy in COPD myotubes increases their diameters. Mitophagy helps to maintain mitochondrial homeostasis by removing impaired mitochondria in COPD. Autophagy is a promising target for improving COPD skeletal muscle dysfunction, and further research should be conducted to elucidate the specific mechanisms by which autophagy mediates COPD skeletal muscle dysfunction, with the aim of enhancing our understanding in this field.
基金Supported by The National Natural Science Foundation of China,No.82103356.
文摘BACKGROUND Improving our understanding of whether increased dietary intake ofω-3 polyunsaturated fatty acids(PUFAs)is beneficial for increasing skeletal muscle mass in patients with metabolic dysfunction-associated fatty liver disease(MAFLD)could provide an important clinical evidence base for the development of relevant nutritional guidelines.AIM To investigate the effect of total dietaryω-3 PUFAs and their subtypes on skeletal muscle mass in MAFLD.METHODS This cross-sectional study involved 2316 participants from four National Health and Nutrition Examination Survey cycles between 2011 and 2018.Dietary intake ofω-3 PUFAs was collected through 24-hour dietary recall interviews.Appendicular skeletal muscle mass index(ASMI)was calculated by dividing ASM in kilograms by height squared.RESULTS The multiple linear regression model showed significant relationships for dietary intake of totalω-3 PUFAs with higher ASMI(β:0.06,95%CI:0.01-0.11)in MAFLD patients.Dietary a-linolenic acid(ALA)(β:0.06,95%CI:0.01-0.12),docosapentaenoic acid(β:1.28,95%CI:0.01-2.54),and docosahexaenoic acid(DHA)(β:0.19,95%CI:0.01-0.37)were significantly associated with higher ASMI,while intake of stearidonic acid and eicosapentaenoic acid did not improve ASMI.In patients with high probability of liver fibrosis,dietary intake of ALA was associated with higher ASMI(β:0.11,95%CI:0.03-0.18).Stratified analysis found that DHA was associated with higher ASMI in patients with obesity and higher metabolic risk.CONCLUSION Increasing dietary intake ofω-3 PUFAs improved skeletal muscle health in patients with MAFLD.Patient with obesity and higher metabolic risk were more likely to benefit from intake of DHA.
基金supported by the Swedish Research Council(201500165)a Wallenberg Scholars Award from the Knut and Alice Wallenberg Foundation(KAW 2023.0312)The Novo Nordisk Foundation Center for Basic Metabolic Research is an independent research center at the University of Copenhagen,partially funded by an unrestricted donation from the Novo Nordisk Foundation(NNF23SA0084103).
文摘1.Exercise enhances muscle function and insulin sensitivity Skeletal muscle plays a fundamental role in not only locomotion,but also systemic metabolism.In people with type 2 diabetes,skeletal muscle is a major site of insulin resistance,with impaired insulin signaling and reduced glucose transport activity contributing to metabolic dysfunction.
基金supported by the National Natural Science Foundation of China(32272895 and 32172744).
文摘Background While maternal proline(Pro)supplementation has demonstrated efficacy in enhancing placental angiogenesis and farrowing efficiency in swine,its regulatory role in fetal skeletal muscle ontogeny remains undefined.This study systematically evaluated the temporal-specific impacts of dietary Pro supplementation during critical phases of fetal myogenesis(encompassing primary myofiber formation and secondary myofiber hyperplasia)on offspring muscle development.A total of 120 sows with similar farrowing schedules were assigned to three groups:CON(basal diet),ST-Pro(0.5%Pro supplementation during secondary myofiber formation period,from d 60 gestation to farrowing),LT-Pro(0.5%Pro supplementation spanning primary and secondary myofiber formation period:from d 20 gestation to farrowing).Results LT-Pro group significantly increased the longissimus dorsi(LD)muscle mass per unit body weight in newborn piglets compared to CON group(P<0.05),while no such effect was observed in the ST-Pro group.Metabolomic profiling revealed elevated Pro,lysine,and tryptophan levels in the LD muscle of LT-Pro group piglets,accompanied by reduced branched-chain amino acids(BCAAs;leucine,isoleucine,and valine)in both serum and muscle(P<0.05).Histological analysis demonstrated a 45.74%increase in myofiber cross-sectional area in the LT-Pro group(P<0.05).At the molecular level,LT-Pro group piglets exhibited upregulated mRNA expression levels of myogenic regulatory genes(MYOD1,MYF6)and the cell cycle accelerator CCND1(P<0.05),coupled with activation of the STAT3 signaling pathway(phosphorylated STAT3 protein increased by 2.53-fold,P<0.01).Furthermore,Pro supplementation enhanced oxidative metabolism,evidenced by elevated mitochondrial biogenesis markers(the mRNA expression levels of PPARGC1A,OPA1,and SQSTM1)and a 61.58%increase in succinate dehydrogenase activity(P<0.05).Notably,LT-Pro group piglets showed a selective shift toward slow-twitch oxidative fibers,with both MyHC1 mRNA and protein expression levels significantly upregulated(P<0.05),while the mRNA expression levels of MyHCIIb showed no significant change.Conclusions This study identified the primary fiber formation period as a critical window.Supplementation with Pro during G20–114 reprogrammed offspring skeletal muscle development through STAT3-CCND1-mediated myoblast proliferation,enhanced mitochondrial bioenergetics,and oxidative fiber specification.However,no such effects were observed during G60–114.These findings propose maternal Pro intervention as a novel strategy to enhance muscle yield and metabolic efficiency in swine production,with potential applications for improving meat quality traits linked to oxidative muscle phenotypes.
文摘Metabolic dysfunction-associated steatotic liver disease is increasingly understood to be closely linked with skeletal muscle alterations,such as sarcopenia,myoste-atosis,and metabolic dysregulation,which play a key role in its pathogenesis and progression.Recent literature,including an article by Isakov,highlights the bidirectional interactions between muscle and liver,underscoring shared mechanisms such as insulin resistance,inflammation,and myokine imbalance.This letter reflects on key findings from the review,noting strengths such as its integration of mechanistic insights,discussion of emerging biomarkers,and emphasis on lifestyle and pharmacological interventions.It also identifies areas for further development,including standardization of diagnostic criteria and more rigorous evaluation of translational data.As muscle health gains promi-nence in metabolic dysfunction-associated steatotic liver disease research,multidisciplinary strategies that target both hepatic and muscular systems may offer more effective avenues for prevention and treatment.
文摘BACKGROUND Skeletal muscle alterations(SMAs)are being increasingly recognized in patients with metabolic dysfunctionassociated steatotic liver disease(MASLD)and appear to be associated with deleterious outcomes in these patients.However,their actual prevalence and pathophysiology remain to be elucidated.AIM To determine the prevalence of SMAs and to assess the significance of circulating myokines as biomarkers in patients with MASLD.METHODS Skeletal muscle strength and muscle mass were measured in a cross-sectional study in a cohort of 62 patients fulfilling MASLD criteria,recruited from the outpatient clinics of a tertiary level hospital.The degree of fibrosis and liver steatosis was studied using abdominal ultrasound and transitional elastography.Anthropometric and metabolic characteristics as well as serum levels of different myokines were also determined in the MASLD cohort.Statistical analysis was performed comparing results according to liver fibrosis and steatosis.RESULTS No significant differences were found in both skeletal muscle strength and skeletal muscle mass in patients with MASLD between different stages of liver fibrosis.Interestingly,serum levels of fibroblast growth factor-21(FGF21)were significantly higher in patients with MASLD with advanced hepatic fibrosis(F3-F4)than in those with lower fibrosis stages(F0-F2)(197.49±198.27 pg/mL vs 95.62±83.67 pg/mL;P=0.049).In addition,patients with MASLD with severe hepatosteatosis(S3)exhibited significantly higher serum levels of irisin(1116.87±1161.86 pg/mL)than those with lower grades(S1-S2)(385.21±375.98 pg/mL;P=0.001).CONCLUSION SMAs were uncommon in the patients with MASLD studied.Higher serum levels of irisin and FGF21 were detected in patients with advanced liver steatosis and fibrosis,respectively,with potential implications as biomarkers.
文摘Background: Aging-induced cardiac hypertrophy and reduced skeletal muscle strength contribute to increased disease risk and life burden in the elderly. FNDC5 acts as a protective muscle factor in both cardiac and skeletal muscle. This study aims to examine the relationship between cardiac FNDC5 and aging-related cardiac hypertrophy and decreased skeletal muscle strength. Methods: Male young C57BL/6 mice (5 months old, n = 6) and aged mice (21 months old, n = 6) were utilized in the study and housed in a specific pathogen-free (SPF) environment. Prior to the experiment, grip strength tests were performed on the mice, and heart tissues were collected for morphological analysis, including the assessment of peroxisome proliferator-activated receptor gamma coactivator 1α (PGC-1α) and fibronectin type III-containing structural domain 5 (FNDC5) protein levels. Furthermore, myosin heavy chain II (MyHC II), skeletal muscle-specific transcription factor (MyoD), muscle RING-finger protein-1 (MuRF1), and FNDC5 levels were evaluated in the quadriceps muscle. The correlations between heart weight and FNDC5 expression levels, as well as skeletal muscle indices in the mice, were subsequently analyzed. Result: Aging leads to cardiac hypertrophy and reduced expression of PGC-1α and FNDC5 proteins. Concurrently, there is a decline in the strength of skeletal muscle, along with decreased expression of MyHC II and increased expression of MURF1 and MyoD. Correlation analysis demonstrated strong positive associations between myocardial FNDC5 protein levels and limb grip strength, as well as MyHC II, and strong negative associations with MyoD and MuRF1. Conclusion: There may be a significant association between aging-induced cardiac hypertrophy and decreased skeletal muscle strength, with FNDC5 potentially playing a crucial role as a regulatory molecule facilitating communication between the heart and skeletal muscle.
基金supported by the National Natural Science Foundation of China(32071166 and 32072254)the Ministry of Science and Technology of China(2022YFF1100502)+2 种基金the Earmarked Fund for China Agriculture Reasearch System(CARS-08-G19)the“Qing Lan Project”of Jiangsu Province and the Young Elite Scientists Sponsorship Program by CAST(2020QNRC001)Fundamental Research Funds for the Central Universities(JUSRP622027)。
文摘Highland barley tea(HBT)is made from roasted barley seeds and is abundant inβ-glucan,amino acids,minerals,phenolics,and other natural active ingredients.These natural compounds found in whole grains have been shown to slow aging and positively affect skeletal muscle function.As a result,studying the effects of HBT on the skeletal muscle health of the elderly population is critical from a scientific and societal standpoint for improving their health status and reducing the medical burden on society.The antioxidant activity and the content of natural active substances were used as indicators to screen the optimal process of HBT brewing.The effects of long-term HBT consumption on aging in mice were investigated by using HBT as a substitute for drinking water in naturally aging mice for a 5-month intervention.Afterward,various factors were measured,such as basic physiological indices,inflammation,plasma metabolites,skeletal muscle function,and exercise capacity,to evaluate the effects of HBT on aging in mice.Long-term consumption of HBT reduced body and spleen weight,increased body weight percentage of skeletal muscle,and reduced plasma inflammation levels in aging mice.Metabolomic results showed increased plasma levels of the mitochondrial marker short-chain acylcarnitine and some amino acids.Additionally,there was a decrease in bile and long-chain acylcarnitine.The level of fibrosis in the gastrocnemius muscle of aging mice was suppressed,and the percentage of typeⅠmuscle fibers was increased,improving the endurance of the mice.Thus,long-term consumption of HBT may reduce body weight and increase skeletal muscle mitochondrial activity and exercise capacity in aging mice by reducing inflammation levels and alleviating mitochondrial damage.
基金Supported by Chongqing Young and Middle-aged Medical High-end Talents,No.YXGD202405Chongqing District and County Head Goose Talents,Chongqing Science and Technology and Health Joint Scientific Research Project on Traditional Chinese Medicine,No.2024ZYYB036Chongqing Banan District Science and Technology and Health Joint Scientific Research Project on Traditional Chinese Medicine,No.BNWJ202300112.
文摘BACKGROUND Many studies have found that sarcopenia is related to the survival of patients with liver cancer,which may lead to worse prognosis.AIM To investigate the relationship between skeletal muscle mass and prognosis in patients with liver cancer receiving targeted therapy by meta-analysis.METHODS PubMed,Embase,Cochrane Library,and Web of Science were searched for clinical studies on the relationship between skeletal muscle index(SMI)and the prognosis of patients with liver cancer receiving targeted therapy from inception to March 1,2022.Meta-analysis and sensitivity analysis of the data were performed using Stata 16.0 software.RESULTS A total of 6877 studies were searched,and finally 12 articles with 1715 cases were included.Meta-analysis result of 8 articles showed that compared with non-low SMI group,the overall survival(OS)of patients with liver cancer in the low SMI group was significantly shorter(hazard ratio=1.60,95%confidence interval:1.44-1.77,P=0.000).Meta-analysis result of 4 articles showed that,compared with low SMI group,patients in the nonlow SMI group had longer OS(hazard ratio=0.59,95%confidence interval:0.38-0.91,P=0.018).CONCLUSION Skeletal muscle mass is positively correlated with OS in patients with liver cancer receiving targeted therapy.
基金supported by the National Natural Science Foundation of China(82003447,32202023)the Natural Science Foundation of Shandong Province(ZR2021QC177)the Young Scholars Program of Shandong University(2018WLJH33,2018WLJH34)。
文摘Obesity is associated with skeletal muscle mass loss and physical dysfunction.Krill oil(KO)has been shown to be beneficial in human health.However,the effect of KO on obesity-induced skeletal muscle atrophy is still unclear.In this study,the male C57BL/6J mice were fed a high-fat diet(HFD)for 12 weeks to induce obesity,and then were intragastric administration with 400 mg/kg bw KO for an additional 6 weeks.The results showed that KO treatment reduced body weight,fat accumulation and serum pro-inflammatory cytokines in HFD-induced obese mice.Importantly,KO treatment attenuated skeletal muscle atrophy in HFD-fed mice,as evidenced by preserving skeletal muscle mass,average myofiber cross-sectional area and grip strength.KO administration also mitigated obesity-induced ectopic lipid deposition and inflammatory response in skeletal muscle.Additionally,KO treatment inhibited the transcriptional activities of nuclear factor-κB(NF-κB)p65 and forkhead box O 3a(FoxO3a),and then down-regulated muscle atrophy F-box(MAFbx)and muscle-specific RING finger protein 1(MuRF1)protein levels in skeletal muscle from HFD-fed mice.KO administration also improved obesity-induced impaired muscle protein synthesis via activating PI3K/Akt pathway.Furthermore,KO treatment enhanced muscle mitochondrial biogenesis in HFD-induced obese mice via activating PGC-1αpathway.Collectively,KO might be developed as a potential nutritional supplement for the prevention and treatment of obesity-induced skeletal muscle atrophy.
基金supported by a grant from the Russian Science Foundation(23-75-01061)。
文摘Objectives:Skeletal muscle ischemia/reperfusion injury(IRI)occurs as a result of a marked reduction in arterial perfusion to a limb and can lead to tissue death and threaten limb viability.This work assessed the effects of 20-hydroxyecdysone(20E)on hindlimb skeletal tissue following tourniquet-induced ischemia/reperfusion injury.Methods:Animals were divided into 4 groups—control group(Control),Control+20E(C+20E),mice with IRI(IRI),and mice with IRI+20E(IRI+20E).IRI was modeled by applying a tourniquet to the hind limb for 2 h with reperfusion for 1 h.5 mg/kg of 20E was administered intraperitoneally for 14 days.Afterward,the physical activity of mice,the histological structure of the quadriceps femoris,the expression of genes encoding proteins induced by hypoxia and involved in tissue adaptation to ischemia,and the functional parameters of skeletal muscle mitochondria were assessed.Results:It was shown that IRI of the limbs leads to functional disorders,depression of muscle function,accumulation of malondialdehyde(MDA)in mitochondria,and a decrease in their Ca2+buffering capacity,as well as an increase in the expression of HIF-1α,VGEF-A,PGC1αand PDGF-BB genes associated with adaptation to ischemia.20E reduced the intensity of degenerative processes in skeletal muscles,which was expressed in a decrease in the number of centrally nucleated fibers.Analysis of gene expression levels indicated a high degree of adaptation of animals to IRI.20E reduced the level of MDA in mitochondria,but did not affect the rate of respiration and calcium retention capacity of organelles both in normal conditions and during IRI.Conclusion:20E partially alleviates the skeletal muscle damage caused by IRI and can be used as part of combination therapy.
文摘The skeletal muscle is the largest organ present in the body and is responsible for mechanical activities like maintaining posture,movement,respiratory function,and support for the health and functioning of other systems of the body.Skeletal muscle atrophy is a condition characterized by a reduction in muscle size,strength,and activity,which leads to an increased dependency on others for movement,an increased risk of falls,and a reduced quality of life.Various conditions like osteoarthritis,osteoporosis,and fractures are directly associated with increased muscle atrophy.Additionally,numerous risk factors,like aging,malnutrition,physical inactivity,and certain disease conditions,through distinct pathways,negatively affect skeletal muscle health and lead to muscle atrophy.Among various determinants of overall muscle health,the rate of muscle protein synthesis and degradation is an important parameter that eventually alters the fate of overall muscle health.In conditions of excessive skeletal muscle atrophy,including sarcopenia,the rate of muscle protein degradation usually exceeds the rate of protein synthesis.The availability of amino acids in the systemic circulation is a crucial step in muscle protein synthesis.The current review aims to consolidate the existing evidence on amino acids,highlight their mechanisms of action,and assess their roles and effectiveness in enhancing skeletal muscle health.
基金supported by the German Research Council(Deutsche Forschungsgemeinschaft,HA3309/3-1/2,HA3309/6-1,HA3309/7-1)。
文摘Skeletal muscles are essential for locomotion,posture,and metabolic regulation.To understand physiological processes,exercise adaptation,and muscle-related disorders,it is critical to understand the molecular pathways that underlie skeletal muscle function.The process of muscle contra ction,orchestrated by a complex interplay of molecular events,is at the core of skeletal muscle function.Muscle contraction is initiated by an action potential and neuromuscular transmission requiring a neuromuscular junction.Within muscle fibers,calcium ions play a critical role in mediating the interaction between actin and myosin filaments that generate force.Regulation of calcium release from the sarcoplasmic reticulum plays a key role in excitation-contraction coupling.The development and growth of skeletal muscle are regulated by a network of molecular pathways collectively known as myogenesis.Myogenic regulators coordinate the diffe rentiation of myoblasts into mature muscle fibers.Signaling pathways regulate muscle protein synthesis and hypertrophy in response to mechanical stimuli and nutrient availability.Seve ral muscle-related diseases,including congenital myasthenic disorders,sarcopenia,muscular dystrophies,and metabolic myopathies,are underpinned by dys regulated molecular pathways in skeletal muscle.Therapeutic interventions aimed at preserving muscle mass and function,enhancing regeneration,and improving metabolic health hold promise by targeting specific molecular pathways.Other molecular signaling pathways in skeletal muscle include the canonical Wnt signaling pathway,a critical regulator of myogenesis,muscle regeneration,and metabolic function,and the Hippo signaling pathway.In recent years,more details have been uncovered about the role of these two pathways during myogenesis and in developing and adult skeletal muscle fibers,and at the neuromuscular junction.In fact,research in the last few years now suggests that these two signaling pathways are interconnected and that they jointly control physiological and pathophysiological processes in muscle fibers.In this review,we will summarize and discuss the data on these two pathways,focusing on their concerted action next to their contribution to skeletal muscle biology.However,an in-depth discussion of the noncanonical Wnt pathway,the fibro/a dipogenic precursors,or the mechanosensory aspects of these pathways is not the focus of this review.
基金Supported by National Natural Science Foundation of China,No.82172509.
文摘BACKGROUND Fibro-adipogenic progenitors(FAPs)are a group of mesenchymal stem cells that cause fibro-fatty degeneration in skeletal muscle in various chronic disease mode-ls.FAPs also play a role in preventing muscle degeneration at acute stages during disease progression.However,few studies have reported the changes in and function of FAPs in the acute phase after tendon rupture.AIM To clarify the changes in the number of FAPs and their impact on skeletal muscle soon after tendon rupture to facilitate future studies targeting FAPs to treat muscle degeneration.METHODS We utilized Pdgfra-H2B::eGFP mice to trace and quantify FAPs in a tibialis anterior tenotomy(TAT)model at 0 and 3 days,1 week,2 weeks,3 weeks,4 weeks,5 weeks,and 6 weeks post-injury,and the results were further validated using fluorescence-activated cell sorting analysis with C57BL/6 mice at the same post-injury timepoints.We subsequently used PdgfraCreERT::RosaDTA mice,and evaluated the severity of post-TAT skeletal muscle degeneration with or without FAP-depletion.RESULTS The number of FAPs peaked at 1 week post-TAT before gradually declining to a level comparable to that pre-TAT.The change in the number of FAPs was potentially temporally correlated with the progression of skeletal muscle degeneration after TAT.FAP-depletion led to more severe degeneration early after TAT,indicating that FAPs potentially alleviate muscle degeneration after tendon rupture in the early post-injury phase.CONCLUSION FAPs potentially alleviate the degeneration of skeletal muscle in the acute stage after tendon rupture.
文摘BACKGROUND Metastasis of renal cell carcinoma(RCC)to the skeletal muscle and small bowel is an exceedingly rare occurrence.Both of these sites are unusual sites for RCC to metastasize to and to occur simultaneously is even less common.CASE SUMMARY A 58-year-old male with known history of RCC presented with a recurrence that was diagnosed through imaging and biopsies.Mucosa abnormalities of small bowel noted during endoscopy were biopsied as well as lesion in the psoas muscle that was noted.CONCLUSION This case report emphasizes that RCC can not only recur but can do so even decades later and present as metastatic foci at atypical sites.
基金the Project of National Famous Old Chinese Medicine Experts Inheritance Studio Construction:the National Project of Taking Inheriting Experience of Prestigious Chinese Physicians Wang Linpeng(No.ZY202275)。
文摘OBJECTIVE:To explore the effect of electroacupuncture on skeletal muscle pain in Parkinson's disease(PD).METHODS:A single-center randomized controlled trial was conducted with sixty patients with Parkinson's disease with skeletal muscle pain were randomly divided into electroacupuncture group and sham acupuncture control group with 30 patients each.The electric acupuncture group was treated with electric acupuncture,while the control group was treated with Park needle pseudoacupuncture.Both groups were treated 5 times a week for a total of 4 weeks,and both groups completed 20 treatments.King's Parkinson's Pain Scale(KPPS)and visual analog scale(VAS)were used before and after treatment to evaluate the pain degree of patients.Realtime shear wave elastography(SWE)and modified Ashworth score(MAS)were used to evaluate the changes of muscle tone.Parkinson's comprehensive Score Scale(MDS-UPDRS,including UPDRS Ⅱ and UPDRS Ⅲ)was used to evaluate exercise ability.Hamilton Depression Scale(HAMD)score was used to evaluate the emotional changes of patients.Spearman correlation analysis was used to explore the correlation between pain degree and muscle tone,exercise ability and emotion.RESULTS:During the study,one case fell off in the control group,and 30 cases were eventually included in the analysis and treatment group and 29 cases in the control group.After treatment,Young's modulus of biceps and quadriceps and shear wave velocity of biceps were decreased in electroacupuncture group compared with before treatment,while KPPS score,VAS score,UPDRS Ⅱ,UPDRS Ⅲ and modified Ashworth score were decreased,with statistical significance(P<0.05).There was no statistical significance in control group(P>0.05).After treatment,KPPS score,VAS score,UPDRS Ⅱ and UPDRS Ⅲ,MAS,HAMD score,Young's modulus of biceps and shear wave velocity in electroacupuncture group were significantly lower than those in control group(P<0.05).Spearman correlation analysis showed that KPPS score was positively correlated with UPDRS Ⅲ(r=0.414,P<0.05).KPPS score was positively correlated with HAMD score(r=0.576,P<0.01).CONCLUSION:Electroacupuncture therapy can effectively improve skeletal muscle pain in patients with Parkinson's disease,reduce the muscle hardness of patients,improve patients'daily life ability,and improve patients'emotional disorders.The degree of skeletal muscle pain in PD patients is correlated with motor ability and emotional disorders,but there is no significant correlation between the degree of skeletal muscle pain and the muscle tone of PD patients.
基金supported by NIH Grants R01NS092651 and R21NS111275-01the Department of Veterans Affairs,BX001148 and BX005899(to PHK)。
文摘Amyotrophic lateral sclerosis is a fatal multisystemic neurodegenerative disease with motor neurons being a primary target.Although progressive weakness is a hallmark feature of amyotrophic lateral sclerosis,there is considerable heterogeneity,including clinical presentation,progression,and the underlying triggers for disease initiation.Based on longitudinal studies with families harboring amyotrophic lateral sclerosis-associated gene mutations,it has become apparent that overt disease is preceded by a prodromal phase,possibly in years,where compensatory mechanisms delay symptom onset.Since 85-90%of amyotrophic lateral sclerosis is sporadic,there is a strong need for identifying biomarkers that can detect this prodromal phase as motor neurons have limited capacity for regeneration.Current Food and Drug Administration-approved therapies work by slowing the degenerative process and are most effective early in the disease.Skeletal muscle,including the neuromuscular junction,manifests abnormalities at the earliest stages of the disease,before motor neuron loss,making it a promising source for identifying biomarkers of the prodromal phase.The accessibility of muscle through biopsy provides a lens into the distal motor system at earlier stages and in real time.The advent of“omics”technology has led to the identification of numerous dysregulated molecules in amyotrophic lateral sclerosis muscle,ranging from coding and non-coding RNAs to proteins and metabolites.This technology has opened the door for identifying biomarkers of disease activity and providing insight into disease mechanisms.A major challenge is correlating the myriad of dysregulated molecules with clinical or histological progression and understanding their relevance to presymptomatic phases of disease.There are two major goals of this review.The first is to summarize some of the biomarkers identified in human amyotrophic lateral sclerosis muscle that have a clinicopathological correlation with disease activity,evidence of a similar dysregulation in the SOD1G93A mouse during presymptomatic stages,and evidence of progressive change during disease progression.The second goal is to review the molecular pathways these biomarkers reflect and their potential role in mitigating or promoting disease progression,and as such,their potential as therapeutic targets in amyotrophic lateral sclerosis.
文摘The“longevity protein”SIRT5 could hold the key to delaying age-related muscle decline.A study led by researchers from the Institute of Zoology(IOZ)of the Chinese Academy of Sciences and Capital Medical University in Beijing reveals that SIRT5 mitigates skeletal muscle aging by blocking pro-inflammatory pathways.Published in Nature Metabolism on March 14,2025,the work identifies SIRT5’s interaction with protein kinase TBK1 as critical to preserving muscle mass and function.
基金supported by the National Natural Science Foundation of China(82074523)the National Natural Youth Science Foundation of China(82004448).
文摘Objective:To investigate the effects of acupotomy on skeletal muscle fibrosis and collagen deposition in a rabbit knee osteoarthritis(KOA)model.Methods: Rabbits(n=18)were randomly divided into control,KOA,and KOA+acupotomy(Apo)groups(n=6).The rabbits in the KOA and Apo groups were modeled using the modified Videman's method for 6 weeks.After modeling,the Apo group was subjected to acupotomy once a week for 3 weeks on the vastus medialis,vastus lateralis,rectus femoris,biceps femoris,and anserine bursa tendons around the knee.The behavior of all animals was recorded,rectus femoris tissue was obtained,and histomorphological changes were observed using Masson staining and transmission electron microscopy.The expression of transforming growth factor-β1(TGF-β1),Smad 3,Smad 7,fibrillar collagen types I(Col-I)and III(Col-III)was detected using Western blot and real-time polymerase chain reaction(RT-PCR).Results: Histological analysis revealed that acupotomy improved the microstructure and reduced the collagen volume fraction of rectus femoris,compared with the KOA group(P=.034).Acupotomy inhibited abnormal collagen deposition by modulating the expression of fibrosis-related proteins and mRNA,thus preventing skeletal muscle fibrosis.Western blot and RT-PCR analysis revealed that in the Apo group,Col-I,and Col-III protein levels were significantly lower than those in the KOA group(both P<.01),same as Col-I and Col-III mRNA levels(P=.0031;P=.0046).Compared with the KOA group,the protein levels of TGF-β1 and Smad 3 were significantly reduced(both P<.01),as were the mRNA levels of TGF-β1 and Smad 3(P=.0007;P=.0011).Conversely,the levels of protein and mRNA of Smad 7 were significantly higher than that in the KOA group(P<.01;P=.0271).Conclusion: Acupotomy could alleviate skeletal muscle fibrosis and delay KOA progress by inhibiting collagen deposition through the TGF-β/Smad pathway in the skeletal muscle of KOA rabbits.
