Cells undergo metabolic reprogramming to adapt to changes in nutrient availability, cellular activity, and transitions in cell states. The balance between glycolysis and mitochondrial respiration is crucial for energy...Cells undergo metabolic reprogramming to adapt to changes in nutrient availability, cellular activity, and transitions in cell states. The balance between glycolysis and mitochondrial respiration is crucial for energy production, and metabolic reprogramming stipulates a shift in such balance to optimize both bioenergetic efficiency and anabolic requirements. Failure in switching bioenergetic dependence can lead to maladaptation and pathogenesis. While cellular degradation is known to recycle precursor molecules for anabolism, its potential role in regulating energy production remains less explored. The bioenergetic switch between glycolysis and mitochondrial respiration involves transcription factors and organelle homeostasis, which are both regulated by the cellular degradation pathways. A growing body of studies has demonstrated that both stem cells and differentiated cells exhibit bioenergetic switch upon perturbations of autophagic activity or endolysosomal processes. Here, we highlighted the current understanding of the interplay between degradation processes, specifically autophagy and endolysosomes, transcription factors, endolysosomal signaling, and mitochondrial homeostasis in shaping cellular bioenergetics. This review aims to summarize the relationship between degradation processes and bioenergetics, providing a foundation for future research to unveil deeper mechanistic insights into bioenergetic regulation.展开更多
Microbiologically influenced corrosion （MIC） is a major cause of corrosion damages, facility failures, and financial losses, making MIC an important research topic. Due to complex microbiological activities and a la...Microbiologically influenced corrosion （MIC） is a major cause of corrosion damages, facility failures, and financial losses, making MIC an important research topic. Due to complex microbiological activities and a lack of deep understanding of the interactions between biofilms and metal surfaces, MIC occurrences and mechanisms are difficult to predict and interpret. Many theories and mechanisms have been pro- posed to explain MIC. In this review, the mechanisms of MIC are discussed using hioenergetics, microbial respiration types, and biofilm extracellular electron transfer （EET）. Two main MIC types, namely EET-MIC and metabolite MIC （M-ME）, are discussed. This brief review provides a state of the art insight into MIC mechanisms and it helps the diagnosis and prediction of occurrences of MIC under anaerobic conditions in the oil and gas industry.展开更多
Alzheimer’s disease （AD） is an increasingly pressing worldwide public-health, social, political and economic concern. Despite significant investment in multiple traditional therapeutic strategies that have achieved...Alzheimer’s disease （AD） is an increasingly pressing worldwide public-health, social, political and economic concern. Despite significant investment in multiple traditional therapeutic strategies that have achieved success in preclinical models addressing the pathological hallmarks of the disease, these efforts have not translated into any effective disease-modifying therapies. This could be because interventions are being tested too late in the disease process. While existing therapies provide symptomatic and clinical benefit, they do not fully address the molecular abnormalities that occur in AD neurons. The pathophysiology of AD is complex; mitochondrial bioenergetic deficits and brain hypometabolism coupled with increased mitochondrial oxidative stress are antecedent and potentially play a causal role in the disease pathogenesis. Dysfunctional mitochondria accumulate from the combination of impaired mitophagy, which can also induce injurious inflammatory responses, and inadequate neuronal mitochondrial biogenesis. Altering the metabolic capacity of the brain by modulating/potentiating its mitochondrial bioenergetics may be a strategy for disease prevention and treatment. We present insights into the mechanisms of mitochondrial dysfunction in AD brain as well as an overview of emerging treatments with the potential to prevent, delay or reverse the neurodegenerative process by targeting mitochondria.展开更多
BACKGROUND The pancreatic islet microcirculation adapts its metabolism to cope with limited oxygen availability and nutrient delivery.In diabetes,the balance between oxygen delivery and consumption is impaired.Insulin...BACKGROUND The pancreatic islet microcirculation adapts its metabolism to cope with limited oxygen availability and nutrient delivery.In diabetes,the balance between oxygen delivery and consumption is impaired.Insulin has been proven to exert complex actions promoting the maintenance of homeostasis of the pancreas under glucotoxicity.AIM To test the hypothesis that insulin administration can improve the integrated pancreatic microcirculatory oxygen profile and bioenergetics.METHODS The pancreatic microcirculatory partial oxygen pressure(PO_(2)),relative hemoglobin(rHb)and hemoglobin oxygen saturation(SO_(2))were evaluated in nondiabetic,type 1 diabetes mellitus(T1DM),and insulin-treated mice.A threedimensional framework was generated to visualize the microcirculatory oxygen profile.Ultrastructural changes in the microvasculature were examined using transmission electron microscopy.An Extracellular Flux Analyzer was used to detect the real-time changes in bioenergetics by measuring the oxygen consumption rate and extracellular acidification rate in islet microvascular endothelial cells(IMECs).RESULTS Significantly lower PO_(2),rHb,and SO_(2) values were observed in T1DM mice than in nondiabetic controls.Insulin administration ameliorated the streptozotocin-induced decreases in these microcirculatory oxygen parameters and improved the mitochondrial ultrastructural abnormalities in IMECs.Bioenergetic profiling revealed that the IMECs did not have spare respiratory capacity.Insulin-treated IMECs exhibited significantly greater basal respiration than glucotoxicity-exposed IMECs(P<0.05).An energy map revealed increased energetic metabolism in insulin-treated IMECs,with significantly increased ATP production,non-mitochondrial respiration,and oxidative metabolism(all P<0.05).Significant negative correlations were revealed between microcirculatory SO_(2) and bioenergetic parameters.CONCLUSION Glucotoxicity deteriorates the integrated pancreatic microcirculatory oxygen profile and bioenergetics,but this deterioration can be reversed by insulin administration.展开更多
Background: The active use of stem and progenitor cells in the therapy of various diseases requires thedevelopment of approaches for targeted modification of their properties. One such approach is the induction of a p...Background: The active use of stem and progenitor cells in the therapy of various diseases requires thedevelopment of approaches for targeted modification of their properties. One such approach is the induction of a prooranti-inflammatory phenotype. Methods: In this study, we investigated the effect of a pro-inflammatoryenvironment in vitro on multipotent mesenchymal stromal cells (MSC) by incubation with lipopolysaccharide (LPS).iCELLigence real-time cell analysis system was used for monitoring cell culture growth. Cell energy metabolism wasassessed using the Seahorse XFp Analyzer. For the rat stroke experiment, we used a photoinduced thrombosis (PT)model;after 24 h of surgery, vehicle or MSC or LPS-treated MSC was injected i.v. With magnetic resonance imaging(MRI) we evaluated the volume of ischemic brain injury. For the effect of MSC on neurological deficit after PT weused three methods: limb placement test, cylinder test, and beam-walking test. Results: LPS exposure led to asignificant increase in cell growth rate and to changes in their energy metabolism: glycolytic activity increasedsignificantly in the MSC, and non-glycolytic acidification also increased, while basic respiratory parameters weremaintained. With MRI we didn’t reveal changes in the volume of brain damage between all rat groups. Neurologicaldeficit was less only with using untreated MSC injection. Conclusion: Using LPS-treated MSC in the therapy ofischemic stroke in rats, we did not observe an increase in the neuroprotective properties of the cells, but instead notedsome decrease in their therapeutic efficacy. We attribute these changes to the formation of a pro-inflammatoryphenotype in MSC.展开更多
Objective: To relate biochemistry of the human physiology with the application of the bioenergetic medicine. Methods:Search about the topic in the last 5 years and present a general view of some biochemical processes ...Objective: To relate biochemistry of the human physiology with the application of the bioenergetic medicine. Methods:Search about the topic in the last 5 years and present a general view of some biochemical processes that allow to apply thebioenergetic medicine, due to the need to open new alternatives based on holistic methods. Conclusions: It was based on the searchof articles in the Virtual Library in Health (Spanish: BVS) and using the key words: bioenergetic medicine, vibration, energy,breathing, chakras, biomagnetism, translated into the quality of life’s improvement and the welfare of human being.展开更多
<strong>Background:</strong> Urban air pollution contributes to lung and cardiovascular system dysfunction, making it a major concern for human health. Its impact on skin integrity, associated with increas...<strong>Background:</strong> Urban air pollution contributes to lung and cardiovascular system dysfunction, making it a major concern for human health. Its impact on skin integrity, associated with increased occurrence of atopic dermatitis, is now recognized, but its cellular mechanisms remain poorly understood. <strong>Objective:</strong> In the present study we aimed at establishing the impact of urban pollutant on mitochondrial dynamics and bioenergetics using the HaCaT cell model. We also sought to establish the protective effect of ECH-5195 (red <em>Panax ginseng</em> extract), standardized in ginsenosides, in reversing pollution-induced mitochondrial defects. <strong>Methods:</strong> Urban pollution exposure was mimicked by 1 h exposure of HaCaT cells with standardized atmospheric particulate matter containing PAHs, nitro-PAHs, PCB congeners, and chlorinated pesticides with a mean particulate diameter of 5.85 μm (SRM1648). <strong>Results:</strong> The presence of urban pollutant in the cultures increased the prevalence of hyperfission by 1.41-fold (p = 0.023) and fission by 1.35 fold (p = 0.006) in the reticular mitochondrial network. ECH-5195 reduced both pollution-induced hyperfission by 0.54-fold (p = 0.004) and fission by 0.68-fold (p = 0.0006) normalizing the mitochondrial reticular network. Pollution exposure was associated with a significant reduction of basal OCR and increased lactate production, pushing the cell to rely on glycolysis for ATP production. When ECH-5195 was used, OCR was significantly increased, and the glycolytic contribution to ATP production was reduced while both oxidative phosphorylation and mitochondrial respiration were increased demonstrating mitochondrial re-engagement in ATP production. <strong>Conclusions:</strong> Pollution exposure was disruptive for both the mitochondrial network dynamics and mitochondrial respiration. Ginsenosides in ECH-5195 efficiently protected both from pollution-induced defects.展开更多
The authors regret that in Fig.2Aa of the article,the images for TPUPPy and TPU-aa in the first column were mistakenly duplicated due to a formatting error.The correct version of Fig.2 is provided below,along with the...The authors regret that in Fig.2Aa of the article,the images for TPUPPy and TPU-aa in the first column were mistakenly duplicated due to a formatting error.The correct version of Fig.2 is provided below,along with the original data for reference.The authors confirm that the rest of the article remains unaffected.展开更多
Mitochondrial metabolism plays a pivotal role in tumor progression,yet effective therapeutic targeting remains constrained by limited tissue penetration and lack of spatiotemporal control.Herein,we present Jahn-Teller...Mitochondrial metabolism plays a pivotal role in tumor progression,yet effective therapeutic targeting remains constrained by limited tissue penetration and lack of spatiotemporal control.Herein,we present Jahn-Teller distortion-engineered,self-propelled nanorobots(IDP@Z@AP)that integrate catalytic oxygen generation,mitochondria-targeted drug delivery,and real-time 3D NIR-Ⅱ photoacoustic(PA)imaging for precision tumor therapy.The nanorobots are fabricated by co-encapsulating a NIR-Ⅱ photothermal agent(IR1048)and a mitochondria-targeting chemotherapeutic(DOX-TPP)within a ZIF-8 framework,followed by in situ anchoring of ultrasmall AuPt bimetallic nanozymes.Pt-induced Jahn-Teller distortion modulates the electronic structure of AuPt,enhancing glucose oxidase-and catalase-like activities.Under NIR-Ⅱ laser irradiation,photothermalenhanced cascade catalysis drives autonomous motion and catalyzes intratumoral O2 generation,facilitating deep tumor infiltration.In vitro studies reveal efficient mitochondrial targeting,resulting in significant mito-chondrial membrane depolarization,intracellular ATP depletion,and suppressed cell migration and invasion.In vivo,3D NIR-Ⅱ PA imaging enables noninvasive visualization of nanorobot biodistribution and real-time mapping of catalytic oxygen generation within tumor tissues.This nanorobotic platform effectively modulates tumor hypoxia and enhances chemotherapeutic delivery to mitochondria,ultimately achieving potent tumor suppres-sion.The work offers a smart,catalytically driven,mitochondria-targeted strategy with real-time therapeutic feedback for subcellular-level cancer therapy.展开更多
Sporadic or late-onset Alzheimer’s disease(LOAD)occurs in 1 of 10 people over 65 years of age and comprises 95%of all AD patients.Unlike early-onset AD,which is caused by defined single gene mutations,the mechanisms ...Sporadic or late-onset Alzheimer’s disease(LOAD)occurs in 1 of 10 people over 65 years of age and comprises 95%of all AD patients.Unlike early-onset AD,which is caused by defined single gene mutations,the mechanisms and events underlying risk for LOAD are not fully understood and no substantial disease-modifying interventions are currently available.Age is the most prominent risk factor for LOAD,and interacting age-related and LOAD-associated factors contribute to its pathogenesis.Among these factors are changes in bioenergetic cell functions,which metabolize substrates and produce energy stored in adenosine triphosphate.展开更多
The impaired differentiation ability of resident cells and disordered immune microenvironment in periodontitis pose a huge challenge for bone regeneration.Herein,we construct a piezoelectric hydrogel to rescue the imp...The impaired differentiation ability of resident cells and disordered immune microenvironment in periodontitis pose a huge challenge for bone regeneration.Herein,we construct a piezoelectric hydrogel to rescue the impaired osteogenic capability and rebuild the regenerative immune microenvironment through bioenergetic activation.Under local mechanical stress,the piezoelectric hydrogel generated piezopotential that initiates osteogenic differentiation of inflammatory periodontal ligament stem cells(PDLSCs)via modulating energy metabolism and promoting adenosine triphosphate(ATP)synthesis.Moreover,it also reshapes an anti-inflammatory and pro-regenerative niche through switching M1 macrophages to the M2 phenotype.The synergy of tilapia gelatin and piezoelectric stimulation enhances in situ regeneration in periodontal inflammatory defects of rats.These findings pave a new pathway for treating periodontitis and other immune-related bone defects through piezoelectric stimulation-enabled energy metabolism modulation and immunomodulation.展开更多
Central nervous system(CNS)neurons typically fail to regenerate their axons after injury leading to neurological impairment.Axonal regeneration is a highly energy-demanding cellular program that requires local mitocho...Central nervous system(CNS)neurons typically fail to regenerate their axons after injury leading to neurological impairment.Axonal regeneration is a highly energy-demanding cellular program that requires local mitochondria to supply most energy within injured axons.Recent emerging lines of evidence have started to reveal that injury-triggered acute mitochondrial damage and local energy crisis contribute to the intrinsic energetic restriction that accounts for axon regeneration failure in the CNS.Characterizing and reprogramming bioenergetic signaling and mitochondrial maintenance after axon injury-ischemia is fundamental for developing therapeutic strategies that can restore local energy metabolism and thus facilitate axon regeneration.Therefore,establishing reliable and reproduc-ible neuronal model platforms is critical for assessing axonal energetic metabolism and regeneration capacity after injury-ischemia.In this focused methodology article,we discuss recent advances in applying cutting-edge microflu-idic chamber devices in combination with state-of-the-art live-neuron imaging tools to monitor axonal regeneration,mitochondrial transport,bioenergetic metabolism,and local protein synthesis in response to injury-ischemic stress in mature CNS neurons.展开更多
Pentadecanoic acid(C15:0)is an odd-chain fatty acid,theβ-oxidation of which yields propionyl-CoA that replenishes succinyl-CoA and tricarboxylic acid cycle flux;higher circulating levels are associated with reduced t...Pentadecanoic acid(C15:0)is an odd-chain fatty acid,theβ-oxidation of which yields propionyl-CoA that replenishes succinyl-CoA and tricarboxylic acid cycle flux;higher circulating levels are associated with reduced type 2 diabetes,cardiovascular disease,metabolic dysfunction-associated steatotic liver disease,and mortality.Summarize the cellular and molecular mechanisms underlying these associations.A comprehensive literature search(2000-2025)identified studies of C15:0’s mechanistic actions in vitro and in vivo,and multi-omics studies focused on receptor binding,signaling cascades,gene expression,and comparative pharmacology.C15:0 is a dual partial peroxisome proliferator-activated receptorα/δagonist.It activates AMP-activated protein kinase,suppresses mechanistic target of rapamycin,and selectively inhibits histone deacetylase 6.It augments succinate-driven complex II respiration,preserves mitochondrial membrane potential,limits reactive oxygen species,and attenuates interleukin-6(IL-6)–triggered Janus kinase 2/signal transducer and activator of transcription 3 and nuclear factor kappa B p65 signaling,lowering monocyte chemoattractant protein-1,tumor necrosis factor-alpha,and IL-6.Across the BioMAP®human-primarycell platform–which tests 12 distinct primary human cell systems such as endothelial cells,fibroblasts,macrophages,and T-cells–C15:0(17μM)produced statistically significant changes in 36 mechanistically diverse biomarkers.This broad,multipathway modulation mirrors the phenotype produced by metformin and rapamycin,yet occurred with no detectable cytotoxicity,paralleling metformin and rapamycin with negligible cytotoxicity.C15:0 engages receptor targets that converge on enhanced lipid oxidation,cellular energetics,and inflammation resolution.Although prospective clinical outcomes are still lacking,the pleiotropic mechanism profile positions C15:0 as a potentially unique nutraceutical or adjunct therapeutic candidate.Further research is warranted to confirm its clinical impacts,optimize dosing,and clarify long-term safety as an essential fatty acid supporting metabolic and immune homeostasis.展开更多
Nonalcoholic fatty liver disease(NAFLD) is today considered the most common form of chronic liver disease, affecting a high proportion of the population worldwide. NAFLD encompasses a large spectrum of liver damage, r...Nonalcoholic fatty liver disease(NAFLD) is today considered the most common form of chronic liver disease, affecting a high proportion of the population worldwide. NAFLD encompasses a large spectrum of liver damage, ranging from simple steatosis to steatohepatitis, advanced fibrosis and cirrhosis. Obesity, hyperglycemia, type 2 diabetes and hypertriglyceridemia are the most important risk factors. The pathogenesis of NAFLD and its progression to fibrosis and chronic liver disease is still unknown. Accumulating evidence indicates that mitochondrial dysfunction plays a key role in the physiopathology of NAFLD, although the mechanisms underlying this dysfunction are still unclear. Oxidative stress is considered an important factor in producing lethal hepatocyte injury associated with NAFLD. Mitochondrial respiratory chain is the main subcellular source of reactive oxygen species(ROS), which may damage mitochondrial proteins, lipids and mitochondrial DNA. Cardiolipin, a phospholipid located at the level of the inner mitochondrial membrane, plays an important role in several reactions and processes involved in mitochondrial bioenergetics as well as in mitochondrial dependent steps of apoptosis. This phospholipid is particularly susceptible to ROS attack. Cardiolipin peroxidation has been associated with mitochondrial dysfunction in multiple tissues in several physiopathological conditions, including NAFLD. In this review, we focus on the potential roles played by oxidative stress and cardiolipin alterations in mitochondrial dysfunction associated with NAFLD.展开更多
Hydrogen exhibits the potential to treat Alzheimer's disease. Stereotactic injection has been previously used as an invasive method of administering active hydrogen, but this method has limitations in clinical pra...Hydrogen exhibits the potential to treat Alzheimer's disease. Stereotactic injection has been previously used as an invasive method of administering active hydrogen, but this method has limitations in clinical practice. In this study, triple transgenic(3×Tg) Alzheimer's disease mice were treated with hydrogen-rich water for 7 months. The results showed that hydrogen-rich water prevented synaptic loss and neuronal death, inhibited senile plaques, and reduced hyperphosphorylated tau and neurofibrillary tangles in 3×Tg Alzheimer's disease mice. In addition, hydrogen-rich water improved brain energy metabolism disorders and intestinal flora imbalances and reduced inflammatory reactions. These findings suggest that hydrogen-rich water is an effective hydrogen donor that can treat Alzheimer's disease. This study was approved by the Animal Ethics and Welfare Committee of Shenzhen University, China(approval No. AEWC-20140615-002) on June 15, 2014.展开更多
Mitochondria are essential cellular organelles critical for generating adenosine triphosphate for cellular homeostasis, as well as various mechanisms that can lead to both necrosis and apoptosis. The field of ＂mi- to...Mitochondria are essential cellular organelles critical for generating adenosine triphosphate for cellular homeostasis, as well as various mechanisms that can lead to both necrosis and apoptosis. The field of ＂mi- tochondrial medicine＂ is emerging in which injury/disease states are targeted therapeutically at the level of the mitochondrion, including specific antioxidants, bioenergetic substrate additions, and membrane uncoupling agents. Consequently, novel mitochondrial transplantation strategies represent a potentially multifactorial therapy leading to increased adenosine triphosphate production, decreased oxidative stress, mitochondrial DNA replacement, improved bioenergetics and tissue sparing. Herein, we describe briefly the history of mitochondrial transplantation and the various techniques used for both in vitro and in vivo delivery, the benefits associated with successful transference into both peripheral and central nervous system tissues, along with caveats and pitfalls that hinder the advancements of this novel therapeutic.展开更多
Changes in the global environment such as ocean acidification （OA） may interact with anthropogenic pollutants including trace metals threatening the integrity of marine ecosystems. We analyze recent studies on the i...Changes in the global environment such as ocean acidification （OA） may interact with anthropogenic pollutants including trace metals threatening the integrity of marine ecosystems. We analyze recent studies on the interactive effects of OA and trace metals on marine organisms with a focus on the physiological basis of these interactions. Our analysis shows that the responses to elevated CO2 and metals are strongly dependent on the species, developmental stage, metal biochemistry and the degree of environmental hypercapnia, and cannot be directly predicted from the CO2-induced changes in metal solubility and speciation. The key physiological functions affected by both the OA and trace metal exposures involve acid-base regulation, pro- tein turnover and mitochondrial bioenergetics, reflecting the sensitivity of the underlying molecular and cellular pathways to CO2 and metals. Physiological interactions between elevated CO2 and metals may impact the organisms＇ capacity to maintain ac- id-base homeostasis and reduce the amount of energy available for fitness-related functions such as growth, development and re- production thereby affecting survival and performance of estuarine populations. Environmental hypercapnia may also affect the marine food webs by altering predator-prey interactions and the trophic transfer of metals in the food chain. However, our under- standing of the degree to which these effects can impact the function and integrity of marine ecosystems is limited due the scar- city of the published research and its bias towards certain taxonomic groups. Future research priorities should include studies of metal x Pco2 interactions focusing on critical physiological functions （including acid-base, protein and energy homeostasis） in a greater range of ecologically and economically important marine species, as well as including the field populations naturally ex- posed （and potentially adapted） to different levels of metals and CO2 in their environments [Current Zoology 61 （4）： 653-668, 2015].展开更多
Cardiogenic shock is the leading cause of death among patients hospitalized with acute myocardial infarction （MI）. Understanding the mechanisms for acute pump failure is therefore important. The aim of this study is...Cardiogenic shock is the leading cause of death among patients hospitalized with acute myocardial infarction （MI）. Understanding the mechanisms for acute pump failure is therefore important. The aim of this study is to examine in an acute MI dog model whether mitochondrial bio-energetic function within non-ischemic wall regions are associated with pump failure. Anterior MI was produced in dogs via ligation of left anterior descending （LAD） coronary artery, that resulted in an infract size of about 30% of the left ventricular wall. Measurements ofhemodynamic status, mitochondrial function, free radical production and mitochondrial uncoupling protein 3 （UCP3） expression were determined over 24 h period. Hemodynamic measurements revealed a 〉 50% reduction in cardiac output at 24 h post infarction when compared to baseline. Biopsy samples were obtained from the posterior non-ischemic wall during acute infarction. ADP/O ratios for isolated mitochondria from non-ischemic myocardium at 6 h and 24 h were decreased when compared to the ADP/O ratios within the same samples with and without palmitic acid （PA）. GTP inhibition of （PA）-stimulated state 4 respiration in isolated mitochondria from the non-ischemic wall increased by 7% and 33% at 6 h and 24 h post-infarction respectively when compared to sham and pre-infarction samples. This would suggest that the mitochondria are uncoupled and this is supported by an associated increase in UCP3 expression observed on western blots from these same biopsy samples. Blood samples from the coronary sinus measured by electron paramagnetic resonance （EPR） methods showed an increase in reactive oxygen species （ROS） over baseline at 6 h and 24 h post-infarction. In conclusion, mitochondrial bio-energetic ADP/O ratios as a result of acute infarction are abnormal within the non-ischemic wall. Mitochondria appear to be energetically uncoupled and this is associated with declining pump function. Free radical production may be associated with the induction of uncoupling proteins in the mitochondria.展开更多
The interest of this conference is agricultural, environmental, bioenergetics, and sanitary. In that context, domestic, agricultural and industrial environments produce organic waste, which needs to be collected, sele...The interest of this conference is agricultural, environmental, bioenergetics, and sanitary. In that context, domestic, agricultural and industrial environments produce organic waste, which needs to be collected, selected, stored and recycled properly in order to avoid environmental pollution and promote agriculture. The green Industry proposed involves the conversion of natural, non-toxic organic waste in order to efficiently produce organic fertilizers for agriculture. These types of fertilizers from biological origin are suitable because they are not toxic for human and the environment. Enzymatic reactions described in this presentation concern mainly the hydrolysis of proteins, sugars and lipids, the acidification of intermediate products from hydrolysis, the formation of acetate, and the production of methane. In other words, this review is timely as it discusses for the chemical behavior or the reactivity of different functional groups to better understand the enzymatic catalysis in the transformations of residual proteins, carbohydrates, and lipids to generate biomethane and fertilizers. In the same perspective, this review is to enrich the documentation related to organic reactions catalyzed by enzymes, which occur in the anaerobic degradation of residual organic substances, with emphasis on the structures of organic compounds and reaction mechanisms. This will allow understanding the displacement of the electrons of a reactive entity rich in electrons to another reactive entity that is poor in electrons to form new bonds in products.展开更多
Background:Adenosine triphosphatase inhibitory factor 1(IF1)is a key protein involved in energy metabolism.IF1 has been linked to various agerelated diseases,although its relationship with physical activity(PA)remains...Background:Adenosine triphosphatase inhibitory factor 1(IF1)is a key protein involved in energy metabolism.IF1 has been linked to various agerelated diseases,although its relationship with physical activity(PA)remains unclear.Additionally,the apolipoprotein A-I(apoA-I),a PA-modulated lipoprotein,could play a role in this relationship because it shares a binding site with IF1 on the cell-surface ATP synthase.We examined here the associations between chronic PA and plasma IF1 concentrations among older adults,and we investigated whether apoA-I mediated these associations.Methods:In the present work,1096 healthy adults(63.8%females)aged 70 years and over who were involved in the Multidomain Alzheimer Prevention Trial study were included.IF1 plasma concentrations(square root of ng/mL)were measured at the 1-year visit of the Multidomain Alzheimer Prevention Trial,while PA levels(square root of metabolic equivalent task min/week)were assessed using questionnaires administered each year from baseline to the 3-year visit.Multiple linear regressions were performed to investigate the associations between the first-year mean PA levels and IF1 concentrations.Mediation analyses were conducted to examine whether apoA-I mediated these associations.Mixedeffect linear regressions were carried out to investigate whether the 1-year visit IF1 concentrations predicted subsequent changes in PA.Results:Multiple linear regressions indicated that first-year mean PA levels were positively associated with IF1 concentrations(B=0.021;SE=0.010;p=0.043).Mediation analyses revealed that about 37.7%of this relationship was mediated by apoA-I(B_(ab)=0.008;SE=0.004;p=0.023).Longitudinal investigations demonstrated that higher concentrations of IF1 at the 1-year visit predicted a faster decline in PA levels over the subsequent 2 years(time×IF1:B=0.148;SE=0.066;p=0.025).Conclusion:This study demonstrates that regular PA is associated with plasma IF1 concentrations,and it suggests that apoA-I partly mediates this association.Additionally,this study finds that baseline concentrations of IF1 can predict future changes in PA.However,further research is needed to fully understand the mechanisms underlying these observations.展开更多
文摘Cells undergo metabolic reprogramming to adapt to changes in nutrient availability, cellular activity, and transitions in cell states. The balance between glycolysis and mitochondrial respiration is crucial for energy production, and metabolic reprogramming stipulates a shift in such balance to optimize both bioenergetic efficiency and anabolic requirements. Failure in switching bioenergetic dependence can lead to maladaptation and pathogenesis. While cellular degradation is known to recycle precursor molecules for anabolism, its potential role in regulating energy production remains less explored. The bioenergetic switch between glycolysis and mitochondrial respiration involves transcription factors and organelle homeostasis, which are both regulated by the cellular degradation pathways. A growing body of studies has demonstrated that both stem cells and differentiated cells exhibit bioenergetic switch upon perturbations of autophagic activity or endolysosomal processes. Here, we highlighted the current understanding of the interplay between degradation processes, specifically autophagy and endolysosomes, transcription factors, endolysosomal signaling, and mitochondrial homeostasis in shaping cellular bioenergetics. This review aims to summarize the relationship between degradation processes and bioenergetics, providing a foundation for future research to unveil deeper mechanistic insights into bioenergetic regulation.
基金supported by Science Foundation of China University of Petroleum,Beijing(Nos.2462017YJRC038 and 2462018BJC005)supported by the National Natural Science Foundation of China(Grant U1660118)+1 种基金the National Basic Research Program of China(973 Program,No.2014CB643300)the National Environmental Corrosion Platform(NECP)
文摘Microbiologically influenced corrosion （MIC） is a major cause of corrosion damages, facility failures, and financial losses, making MIC an important research topic. Due to complex microbiological activities and a lack of deep understanding of the interactions between biofilms and metal surfaces, MIC occurrences and mechanisms are difficult to predict and interpret. Many theories and mechanisms have been pro- posed to explain MIC. In this review, the mechanisms of MIC are discussed using hioenergetics, microbial respiration types, and biofilm extracellular electron transfer （EET）. Two main MIC types, namely EET-MIC and metabolite MIC （M-ME）, are discussed. This brief review provides a state of the art insight into MIC mechanisms and it helps the diagnosis and prediction of occurrences of MIC under anaerobic conditions in the oil and gas industry.
文摘Alzheimer’s disease （AD） is an increasingly pressing worldwide public-health, social, political and economic concern. Despite significant investment in multiple traditional therapeutic strategies that have achieved success in preclinical models addressing the pathological hallmarks of the disease, these efforts have not translated into any effective disease-modifying therapies. This could be because interventions are being tested too late in the disease process. While existing therapies provide symptomatic and clinical benefit, they do not fully address the molecular abnormalities that occur in AD neurons. The pathophysiology of AD is complex; mitochondrial bioenergetic deficits and brain hypometabolism coupled with increased mitochondrial oxidative stress are antecedent and potentially play a causal role in the disease pathogenesis. Dysfunctional mitochondria accumulate from the combination of impaired mitophagy, which can also induce injurious inflammatory responses, and inadequate neuronal mitochondrial biogenesis. Altering the metabolic capacity of the brain by modulating/potentiating its mitochondrial bioenergetics may be a strategy for disease prevention and treatment. We present insights into the mechanisms of mitochondrial dysfunction in AD brain as well as an overview of emerging treatments with the potential to prevent, delay or reverse the neurodegenerative process by targeting mitochondria.
基金Supported by the Beijing Municipal Natural Science Foundation,No.7212068the National Natural Science Foundation of China,No.81900747.
文摘BACKGROUND The pancreatic islet microcirculation adapts its metabolism to cope with limited oxygen availability and nutrient delivery.In diabetes,the balance between oxygen delivery and consumption is impaired.Insulin has been proven to exert complex actions promoting the maintenance of homeostasis of the pancreas under glucotoxicity.AIM To test the hypothesis that insulin administration can improve the integrated pancreatic microcirculatory oxygen profile and bioenergetics.METHODS The pancreatic microcirculatory partial oxygen pressure(PO_(2)),relative hemoglobin(rHb)and hemoglobin oxygen saturation(SO_(2))were evaluated in nondiabetic,type 1 diabetes mellitus(T1DM),and insulin-treated mice.A threedimensional framework was generated to visualize the microcirculatory oxygen profile.Ultrastructural changes in the microvasculature were examined using transmission electron microscopy.An Extracellular Flux Analyzer was used to detect the real-time changes in bioenergetics by measuring the oxygen consumption rate and extracellular acidification rate in islet microvascular endothelial cells(IMECs).RESULTS Significantly lower PO_(2),rHb,and SO_(2) values were observed in T1DM mice than in nondiabetic controls.Insulin administration ameliorated the streptozotocin-induced decreases in these microcirculatory oxygen parameters and improved the mitochondrial ultrastructural abnormalities in IMECs.Bioenergetic profiling revealed that the IMECs did not have spare respiratory capacity.Insulin-treated IMECs exhibited significantly greater basal respiration than glucotoxicity-exposed IMECs(P<0.05).An energy map revealed increased energetic metabolism in insulin-treated IMECs,with significantly increased ATP production,non-mitochondrial respiration,and oxidative metabolism(all P<0.05).Significant negative correlations were revealed between microcirculatory SO_(2) and bioenergetic parameters.CONCLUSION Glucotoxicity deteriorates the integrated pancreatic microcirculatory oxygen profile and bioenergetics,but this deterioration can be reversed by insulin administration.
基金supported by Russian science foundation(grant 21-75-30009).
文摘Background: The active use of stem and progenitor cells in the therapy of various diseases requires thedevelopment of approaches for targeted modification of their properties. One such approach is the induction of a prooranti-inflammatory phenotype. Methods: In this study, we investigated the effect of a pro-inflammatoryenvironment in vitro on multipotent mesenchymal stromal cells (MSC) by incubation with lipopolysaccharide (LPS).iCELLigence real-time cell analysis system was used for monitoring cell culture growth. Cell energy metabolism wasassessed using the Seahorse XFp Analyzer. For the rat stroke experiment, we used a photoinduced thrombosis (PT)model;after 24 h of surgery, vehicle or MSC or LPS-treated MSC was injected i.v. With magnetic resonance imaging(MRI) we evaluated the volume of ischemic brain injury. For the effect of MSC on neurological deficit after PT weused three methods: limb placement test, cylinder test, and beam-walking test. Results: LPS exposure led to asignificant increase in cell growth rate and to changes in their energy metabolism: glycolytic activity increasedsignificantly in the MSC, and non-glycolytic acidification also increased, while basic respiratory parameters weremaintained. With MRI we didn’t reveal changes in the volume of brain damage between all rat groups. Neurologicaldeficit was less only with using untreated MSC injection. Conclusion: Using LPS-treated MSC in the therapy ofischemic stroke in rats, we did not observe an increase in the neuroprotective properties of the cells, but instead notedsome decrease in their therapeutic efficacy. We attribute these changes to the formation of a pro-inflammatoryphenotype in MSC.
文摘Objective: To relate biochemistry of the human physiology with the application of the bioenergetic medicine. Methods:Search about the topic in the last 5 years and present a general view of some biochemical processes that allow to apply thebioenergetic medicine, due to the need to open new alternatives based on holistic methods. Conclusions: It was based on the searchof articles in the Virtual Library in Health (Spanish: BVS) and using the key words: bioenergetic medicine, vibration, energy,breathing, chakras, biomagnetism, translated into the quality of life’s improvement and the welfare of human being.
文摘<strong>Background:</strong> Urban air pollution contributes to lung and cardiovascular system dysfunction, making it a major concern for human health. Its impact on skin integrity, associated with increased occurrence of atopic dermatitis, is now recognized, but its cellular mechanisms remain poorly understood. <strong>Objective:</strong> In the present study we aimed at establishing the impact of urban pollutant on mitochondrial dynamics and bioenergetics using the HaCaT cell model. We also sought to establish the protective effect of ECH-5195 (red <em>Panax ginseng</em> extract), standardized in ginsenosides, in reversing pollution-induced mitochondrial defects. <strong>Methods:</strong> Urban pollution exposure was mimicked by 1 h exposure of HaCaT cells with standardized atmospheric particulate matter containing PAHs, nitro-PAHs, PCB congeners, and chlorinated pesticides with a mean particulate diameter of 5.85 μm (SRM1648). <strong>Results:</strong> The presence of urban pollutant in the cultures increased the prevalence of hyperfission by 1.41-fold (p = 0.023) and fission by 1.35 fold (p = 0.006) in the reticular mitochondrial network. ECH-5195 reduced both pollution-induced hyperfission by 0.54-fold (p = 0.004) and fission by 0.68-fold (p = 0.0006) normalizing the mitochondrial reticular network. Pollution exposure was associated with a significant reduction of basal OCR and increased lactate production, pushing the cell to rely on glycolysis for ATP production. When ECH-5195 was used, OCR was significantly increased, and the glycolytic contribution to ATP production was reduced while both oxidative phosphorylation and mitochondrial respiration were increased demonstrating mitochondrial re-engagement in ATP production. <strong>Conclusions:</strong> Pollution exposure was disruptive for both the mitochondrial network dynamics and mitochondrial respiration. Ginsenosides in ECH-5195 efficiently protected both from pollution-induced defects.
文摘The authors regret that in Fig.2Aa of the article,the images for TPUPPy and TPU-aa in the first column were mistakenly duplicated due to a formatting error.The correct version of Fig.2 is provided below,along with the original data for reference.The authors confirm that the rest of the article remains unaffected.
基金financially supported by the National Natural Science Foundation of China Regional Innovation and Development Joint Fund(Sichuan)(NSFC,No.U21A20417)the 135 Project for Disciplines of Excellence,West China Hospital,Sichuan University(ZYGD24003 and ZYGD23023)the Opening Project of Medical Imaging Key Laboratory of Sichuan Province,North Sichuan Medical College(MIKL202403)。
文摘Mitochondrial metabolism plays a pivotal role in tumor progression,yet effective therapeutic targeting remains constrained by limited tissue penetration and lack of spatiotemporal control.Herein,we present Jahn-Teller distortion-engineered,self-propelled nanorobots(IDP@Z@AP)that integrate catalytic oxygen generation,mitochondria-targeted drug delivery,and real-time 3D NIR-Ⅱ photoacoustic(PA)imaging for precision tumor therapy.The nanorobots are fabricated by co-encapsulating a NIR-Ⅱ photothermal agent(IR1048)and a mitochondria-targeting chemotherapeutic(DOX-TPP)within a ZIF-8 framework,followed by in situ anchoring of ultrasmall AuPt bimetallic nanozymes.Pt-induced Jahn-Teller distortion modulates the electronic structure of AuPt,enhancing glucose oxidase-and catalase-like activities.Under NIR-Ⅱ laser irradiation,photothermalenhanced cascade catalysis drives autonomous motion and catalyzes intratumoral O2 generation,facilitating deep tumor infiltration.In vitro studies reveal efficient mitochondrial targeting,resulting in significant mito-chondrial membrane depolarization,intracellular ATP depletion,and suppressed cell migration and invasion.In vivo,3D NIR-Ⅱ PA imaging enables noninvasive visualization of nanorobot biodistribution and real-time mapping of catalytic oxygen generation within tumor tissues.This nanorobotic platform effectively modulates tumor hypoxia and enhances chemotherapeutic delivery to mitochondria,ultimately achieving potent tumor suppres-sion.The work offers a smart,catalytically driven,mitochondria-targeted strategy with real-time therapeutic feedback for subcellular-level cancer therapy.
文摘Sporadic or late-onset Alzheimer’s disease(LOAD)occurs in 1 of 10 people over 65 years of age and comprises 95%of all AD patients.Unlike early-onset AD,which is caused by defined single gene mutations,the mechanisms and events underlying risk for LOAD are not fully understood and no substantial disease-modifying interventions are currently available.Age is the most prominent risk factor for LOAD,and interacting age-related and LOAD-associated factors contribute to its pathogenesis.Among these factors are changes in bioenergetic cell functions,which metabolize substrates and produce energy stored in adenosine triphosphate.
基金grants from the National Natural Science Foundation of China(82271024,82072065,82202333)National Clinical Key Specialty(Z155080000004)+5 种基金Science and Technology Commission of Shanghai Municipality(22DZ2201300)Shanghai Pujiang Programme(23PJD050)Innovative Research Team of High-level Local Universities in Shanghai(SHSMU-ZLCX20212400)Research Discipline fund(KQXJXK2023)from Ninth People’s Hospital,Shanghai Jiao Tong University School of Medicine,and College of Stomatology,Shanghai Jiao Tong University,the Strategic Priority Research Program of the Chinese Academy of Sciences(No.XDA16021103)the Fundamental Research Funds for the Central Universities(E2EG6802X2,E2E46801)the National Youth Talent Support Program.
文摘The impaired differentiation ability of resident cells and disordered immune microenvironment in periodontitis pose a huge challenge for bone regeneration.Herein,we construct a piezoelectric hydrogel to rescue the impaired osteogenic capability and rebuild the regenerative immune microenvironment through bioenergetic activation.Under local mechanical stress,the piezoelectric hydrogel generated piezopotential that initiates osteogenic differentiation of inflammatory periodontal ligament stem cells(PDLSCs)via modulating energy metabolism and promoting adenosine triphosphate(ATP)synthesis.Moreover,it also reshapes an anti-inflammatory and pro-regenerative niche through switching M1 macrophages to the M2 phenotype.The synergy of tilapia gelatin and piezoelectric stimulation enhances in situ regeneration in periodontal inflammatory defects of rats.These findings pave a new pathway for treating periodontitis and other immune-related bone defects through piezoelectric stimulation-enabled energy metabolism modulation and immunomodulation.
基金This work was supported by grants from the“Young Talent Support Plan”of Xi’an Jiaotong University(71211222010704)to N.Huangthe Intramural Research Program of NINDS,NIH(ZIA NS003029 and ZIA NS002946)to Z.-H.Sheng.
文摘Central nervous system(CNS)neurons typically fail to regenerate their axons after injury leading to neurological impairment.Axonal regeneration is a highly energy-demanding cellular program that requires local mitochondria to supply most energy within injured axons.Recent emerging lines of evidence have started to reveal that injury-triggered acute mitochondrial damage and local energy crisis contribute to the intrinsic energetic restriction that accounts for axon regeneration failure in the CNS.Characterizing and reprogramming bioenergetic signaling and mitochondrial maintenance after axon injury-ischemia is fundamental for developing therapeutic strategies that can restore local energy metabolism and thus facilitate axon regeneration.Therefore,establishing reliable and reproduc-ible neuronal model platforms is critical for assessing axonal energetic metabolism and regeneration capacity after injury-ischemia.In this focused methodology article,we discuss recent advances in applying cutting-edge microflu-idic chamber devices in combination with state-of-the-art live-neuron imaging tools to monitor axonal regeneration,mitochondrial transport,bioenergetic metabolism,and local protein synthesis in response to injury-ischemic stress in mature CNS neurons.
文摘Pentadecanoic acid(C15:0)is an odd-chain fatty acid,theβ-oxidation of which yields propionyl-CoA that replenishes succinyl-CoA and tricarboxylic acid cycle flux;higher circulating levels are associated with reduced type 2 diabetes,cardiovascular disease,metabolic dysfunction-associated steatotic liver disease,and mortality.Summarize the cellular and molecular mechanisms underlying these associations.A comprehensive literature search(2000-2025)identified studies of C15:0’s mechanistic actions in vitro and in vivo,and multi-omics studies focused on receptor binding,signaling cascades,gene expression,and comparative pharmacology.C15:0 is a dual partial peroxisome proliferator-activated receptorα/δagonist.It activates AMP-activated protein kinase,suppresses mechanistic target of rapamycin,and selectively inhibits histone deacetylase 6.It augments succinate-driven complex II respiration,preserves mitochondrial membrane potential,limits reactive oxygen species,and attenuates interleukin-6(IL-6)–triggered Janus kinase 2/signal transducer and activator of transcription 3 and nuclear factor kappa B p65 signaling,lowering monocyte chemoattractant protein-1,tumor necrosis factor-alpha,and IL-6.Across the BioMAP®human-primarycell platform–which tests 12 distinct primary human cell systems such as endothelial cells,fibroblasts,macrophages,and T-cells–C15:0(17μM)produced statistically significant changes in 36 mechanistically diverse biomarkers.This broad,multipathway modulation mirrors the phenotype produced by metformin and rapamycin,yet occurred with no detectable cytotoxicity,paralleling metformin and rapamycin with negligible cytotoxicity.C15:0 engages receptor targets that converge on enhanced lipid oxidation,cellular energetics,and inflammation resolution.Although prospective clinical outcomes are still lacking,the pleiotropic mechanism profile positions C15:0 as a potentially unique nutraceutical or adjunct therapeutic candidate.Further research is warranted to confirm its clinical impacts,optimize dosing,and clarify long-term safety as an essential fatty acid supporting metabolic and immune homeostasis.
文摘Nonalcoholic fatty liver disease(NAFLD) is today considered the most common form of chronic liver disease, affecting a high proportion of the population worldwide. NAFLD encompasses a large spectrum of liver damage, ranging from simple steatosis to steatohepatitis, advanced fibrosis and cirrhosis. Obesity, hyperglycemia, type 2 diabetes and hypertriglyceridemia are the most important risk factors. The pathogenesis of NAFLD and its progression to fibrosis and chronic liver disease is still unknown. Accumulating evidence indicates that mitochondrial dysfunction plays a key role in the physiopathology of NAFLD, although the mechanisms underlying this dysfunction are still unclear. Oxidative stress is considered an important factor in producing lethal hepatocyte injury associated with NAFLD. Mitochondrial respiratory chain is the main subcellular source of reactive oxygen species(ROS), which may damage mitochondrial proteins, lipids and mitochondrial DNA. Cardiolipin, a phospholipid located at the level of the inner mitochondrial membrane, plays an important role in several reactions and processes involved in mitochondrial bioenergetics as well as in mitochondrial dependent steps of apoptosis. This phospholipid is particularly susceptible to ROS attack. Cardiolipin peroxidation has been associated with mitochondrial dysfunction in multiple tissues in several physiopathological conditions, including NAFLD. In this review, we focus on the potential roles played by oxidative stress and cardiolipin alterations in mitochondrial dysfunction associated with NAFLD.
基金supported by the National Natural Science Foundation of China,No.21771126(to XBD)the Shenzhen Bureau of Science,Technology and Information of China,No.JCYJ20180305124000597(to XBD)。
文摘Hydrogen exhibits the potential to treat Alzheimer's disease. Stereotactic injection has been previously used as an invasive method of administering active hydrogen, but this method has limitations in clinical practice. In this study, triple transgenic(3×Tg) Alzheimer's disease mice were treated with hydrogen-rich water for 7 months. The results showed that hydrogen-rich water prevented synaptic loss and neuronal death, inhibited senile plaques, and reduced hyperphosphorylated tau and neurofibrillary tangles in 3×Tg Alzheimer's disease mice. In addition, hydrogen-rich water improved brain energy metabolism disorders and intestinal flora imbalances and reduced inflammatory reactions. These findings suggest that hydrogen-rich water is an effective hydrogen donor that can treat Alzheimer's disease. This study was approved by the Animal Ethics and Welfare Committee of Shenzhen University, China(approval No. AEWC-20140615-002) on June 15, 2014.
基金funded by NIH R21NS096670(AGR)University of Kentucky Spinal Cord and Brain Injury Research Center Chair Endowment(AGR),NIH/NINDS 2P30NS051220
文摘Mitochondria are essential cellular organelles critical for generating adenosine triphosphate for cellular homeostasis, as well as various mechanisms that can lead to both necrosis and apoptosis. The field of ＂mi- tochondrial medicine＂ is emerging in which injury/disease states are targeted therapeutically at the level of the mitochondrion, including specific antioxidants, bioenergetic substrate additions, and membrane uncoupling agents. Consequently, novel mitochondrial transplantation strategies represent a potentially multifactorial therapy leading to increased adenosine triphosphate production, decreased oxidative stress, mitochondrial DNA replacement, improved bioenergetics and tissue sparing. Herein, we describe briefly the history of mitochondrial transplantation and the various techniques used for both in vitro and in vivo delivery, the benefits associated with successful transference into both peripheral and central nervous system tissues, along with caveats and pitfalls that hinder the advancements of this novel therapeutic.
基金This work was in part supported by funds provided by the National Science Foundation award I0S-095107 and UNC Charlotte＇s Faculty Research Grant to I.M.S.
文摘Changes in the global environment such as ocean acidification （OA） may interact with anthropogenic pollutants including trace metals threatening the integrity of marine ecosystems. We analyze recent studies on the interactive effects of OA and trace metals on marine organisms with a focus on the physiological basis of these interactions. Our analysis shows that the responses to elevated CO2 and metals are strongly dependent on the species, developmental stage, metal biochemistry and the degree of environmental hypercapnia, and cannot be directly predicted from the CO2-induced changes in metal solubility and speciation. The key physiological functions affected by both the OA and trace metal exposures involve acid-base regulation, pro- tein turnover and mitochondrial bioenergetics, reflecting the sensitivity of the underlying molecular and cellular pathways to CO2 and metals. Physiological interactions between elevated CO2 and metals may impact the organisms＇ capacity to maintain ac- id-base homeostasis and reduce the amount of energy available for fitness-related functions such as growth, development and re- production thereby affecting survival and performance of estuarine populations. Environmental hypercapnia may also affect the marine food webs by altering predator-prey interactions and the trophic transfer of metals in the food chain. However, our under- standing of the degree to which these effects can impact the function and integrity of marine ecosystems is limited due the scar- city of the published research and its bias towards certain taxonomic groups. Future research priorities should include studies of metal x Pco2 interactions focusing on critical physiological functions （including acid-base, protein and energy homeostasis） in a greater range of ecologically and economically important marine species, as well as including the field populations naturally ex- posed （and potentially adapted） to different levels of metals and CO2 in their environments [Current Zoology 61 （4）： 653-668, 2015].
文摘Cardiogenic shock is the leading cause of death among patients hospitalized with acute myocardial infarction （MI）. Understanding the mechanisms for acute pump failure is therefore important. The aim of this study is to examine in an acute MI dog model whether mitochondrial bio-energetic function within non-ischemic wall regions are associated with pump failure. Anterior MI was produced in dogs via ligation of left anterior descending （LAD） coronary artery, that resulted in an infract size of about 30% of the left ventricular wall. Measurements ofhemodynamic status, mitochondrial function, free radical production and mitochondrial uncoupling protein 3 （UCP3） expression were determined over 24 h period. Hemodynamic measurements revealed a 〉 50% reduction in cardiac output at 24 h post infarction when compared to baseline. Biopsy samples were obtained from the posterior non-ischemic wall during acute infarction. ADP/O ratios for isolated mitochondria from non-ischemic myocardium at 6 h and 24 h were decreased when compared to the ADP/O ratios within the same samples with and without palmitic acid （PA）. GTP inhibition of （PA）-stimulated state 4 respiration in isolated mitochondria from the non-ischemic wall increased by 7% and 33% at 6 h and 24 h post-infarction respectively when compared to sham and pre-infarction samples. This would suggest that the mitochondria are uncoupled and this is supported by an associated increase in UCP3 expression observed on western blots from these same biopsy samples. Blood samples from the coronary sinus measured by electron paramagnetic resonance （EPR） methods showed an increase in reactive oxygen species （ROS） over baseline at 6 h and 24 h post-infarction. In conclusion, mitochondrial bio-energetic ADP/O ratios as a result of acute infarction are abnormal within the non-ischemic wall. Mitochondria appear to be energetically uncoupled and this is associated with declining pump function. Free radical production may be associated with the induction of uncoupling proteins in the mitochondria.
文摘The interest of this conference is agricultural, environmental, bioenergetics, and sanitary. In that context, domestic, agricultural and industrial environments produce organic waste, which needs to be collected, selected, stored and recycled properly in order to avoid environmental pollution and promote agriculture. The green Industry proposed involves the conversion of natural, non-toxic organic waste in order to efficiently produce organic fertilizers for agriculture. These types of fertilizers from biological origin are suitable because they are not toxic for human and the environment. Enzymatic reactions described in this presentation concern mainly the hydrolysis of proteins, sugars and lipids, the acidification of intermediate products from hydrolysis, the formation of acetate, and the production of methane. In other words, this review is timely as it discusses for the chemical behavior or the reactivity of different functional groups to better understand the enzymatic catalysis in the transformations of residual proteins, carbohydrates, and lipids to generate biomethane and fertilizers. In the same perspective, this review is to enrich the documentation related to organic reactions catalyzed by enzymes, which occur in the anaerobic degradation of residual organic substances, with emphasis on the structures of organic compounds and reaction mechanisms. This will allow understanding the displacement of the electrons of a reactive entity rich in electrons to another reactive entity that is poor in electrons to form new bonds in products.
基金supported by grants from the Region Occitanie/Pyrénées-Méditerranée(Grant No.1901175)the European Regional Development Fund(ERDF)(Grant No.MP0022856)+4 种基金This study received funding from la Fédération Française de Cardiologie”(FFC,Dotation Recherche),Alzheimer Prevention in Occitania and Catalonia(APOC Chair of Excellence-Inspire Program)Saint Louis University.The MAPT study was supported by grants from the Gérontopôle of Toulouse,the French Ministry of Health(PHRC 2008,2009)Pierre Fabre Research Institute(manufacturer of the omega-3 supplement)ExonHit Therapeutics SA,and Avid Radiopharmaceuticals,Inc.The promotion of this study was supported by the University Hospital Center of ToulouseThe data-sharing activity was supported by the Association Monegasque pour la Recherche sur la Maladie d'Alzheimer(AMPA)and the INSERM-University of Toulouse III UMR 1295(CERPOP)Research Unit.
文摘Background:Adenosine triphosphatase inhibitory factor 1(IF1)is a key protein involved in energy metabolism.IF1 has been linked to various agerelated diseases,although its relationship with physical activity(PA)remains unclear.Additionally,the apolipoprotein A-I(apoA-I),a PA-modulated lipoprotein,could play a role in this relationship because it shares a binding site with IF1 on the cell-surface ATP synthase.We examined here the associations between chronic PA and plasma IF1 concentrations among older adults,and we investigated whether apoA-I mediated these associations.Methods:In the present work,1096 healthy adults(63.8%females)aged 70 years and over who were involved in the Multidomain Alzheimer Prevention Trial study were included.IF1 plasma concentrations(square root of ng/mL)were measured at the 1-year visit of the Multidomain Alzheimer Prevention Trial,while PA levels(square root of metabolic equivalent task min/week)were assessed using questionnaires administered each year from baseline to the 3-year visit.Multiple linear regressions were performed to investigate the associations between the first-year mean PA levels and IF1 concentrations.Mediation analyses were conducted to examine whether apoA-I mediated these associations.Mixedeffect linear regressions were carried out to investigate whether the 1-year visit IF1 concentrations predicted subsequent changes in PA.Results:Multiple linear regressions indicated that first-year mean PA levels were positively associated with IF1 concentrations(B=0.021;SE=0.010;p=0.043).Mediation analyses revealed that about 37.7%of this relationship was mediated by apoA-I(B_(ab)=0.008;SE=0.004;p=0.023).Longitudinal investigations demonstrated that higher concentrations of IF1 at the 1-year visit predicted a faster decline in PA levels over the subsequent 2 years(time×IF1:B=0.148;SE=0.066;p=0.025).Conclusion:This study demonstrates that regular PA is associated with plasma IF1 concentrations,and it suggests that apoA-I partly mediates this association.Additionally,this study finds that baseline concentrations of IF1 can predict future changes in PA.However,further research is needed to fully understand the mechanisms underlying these observations.
