Age-associated changes in cardiovascular structure/ function are implicated in the markedly increased risk for cardiovascular disease in older persons. Aging not only prolongs exposure to several other cardiovascular ...Age-associated changes in cardiovascular structure/ function are implicated in the markedly increased risk for cardiovascular disease in older persons. Aging not only prolongs exposure to several other cardiovascular risks, but also leads to intrinsic cardiac changes, which reduces cardiac functional reserve, predisposes the heart to stress and contributes to increased cardiovascular mortality in the elderly. Intrinsic cardiac aging in the murine model closely recapitulates age-related cardiac changes in humans, includ- ing left ventricular hypertrophy, fibrosis and diastolic dysfunction. Cardiac aging in mice is accompanied by accumulation of mitochondrial protein oxidation, increased mitochondrial DNA mutations, increased mitochondrial biogenesis, as well as decreased cardiac SERCA2 protein. All of these age-related changes are significantly attenu- ated in mice overexpressing catalase targeted to mitochondria （mCAT）. These findings demonstrate the critical role of rnitochondrial reactive oxygen species （ROS） in cardiac ag ing and support the potential antioxidants to cardiac aging lar diseases. application of mitochondrial and age-related cardiovascular diseases.展开更多
The literature is full of claims regarding the consumption of polyphenol or polyamine-rich foods that offer some protection from developing cardiovascular disease(CVD). This is achieved by preventing cardiac hypertrop...The literature is full of claims regarding the consumption of polyphenol or polyamine-rich foods that offer some protection from developing cardiovascular disease(CVD). This is achieved by preventing cardiac hypertrophy and protecting blood vessels through improving the function of endothelium. However, do these interventions work in the aged human hearts? Cardiac aging is accompanied by an increase in left ventricular hypertrophy, along with diastolic and systolic dysfunction. It also confers significant cardiovascular risks for both sexes. The incidence and prevalence of CVD increase sharply at an earlier age in men than women. Furthermore, the patterns of heart failure differ between sexes, as do the lifetime risk factors. Do caloric restriction(CR)-mimetics, rich in polyphenol or polyamine, delay or reverse cardiac aging equally in both men and women? This review will discuss three areas:(1) mechanisms underlying age-related cardiac remodeling;(2) gender-related differences and potential mechanisms underlying diminished cardiac response in older men and women;(3) we select a few polyphenol or polyamine rich compounds as the CRmimetics, such as resveratrol, quercetin, curcumin, epigallocatechin gallate and spermidine, due to their capability to extend health-span and induce autophagy. We outline their abilities and issues on retarding aging in animal hearts and preventing CVD in humans. We discuss the confounding factors that should be considered for developing therapeutic strategies against cardiac aging in humans.展开更多
Presenilin(Psn)protein is associated with organismal aging.Mutations in the Psn gene may lead to Alzheimer’s disease(AD),dilated cardiomyopathy(DCM),and many age-dependent degenerative diseases.These diseases serious...Presenilin(Psn)protein is associated with organismal aging.Mutations in the Psn gene may lead to Alzheimer’s disease(AD),dilated cardiomyopathy(DCM),and many age-dependent degenerative diseases.These diseases seriously affect the quality of life and longevity of the population and place a huge burden on health care and economic systems around the world.Humans have two types of Psn,presenilin-1(PSEN1)and presenilin-2(PSEN2).Mutations in the genes encoding PSEN1,PSEN2,and amyloid precursor protein(APP)have been identified as the major genetic causes of AD.Psn is a complex gene strongly influenced by genetic and environmental factors.The effects of exercise,training,and a high-fat diet on the Psn gene expressed in the heart and its related pathways are not fully understood.Fortunately,relevant aspects of the mutational effects on Psn can be studied experimentally in easily handled animal models,including Drosophila,mice,and other animals,all of which share orthologous genes of Psn with humans.Many previous studies have linked aging,exercise training,and a high-fat diet to the Psn gene.This review discusses the interrelationship between aging,exercise training,and a high-fat diet on the Psn gene and its associated disease,AD.The aim is to understand the adverse effects of Psn gene mutations on the body and the diseases caused by AD,find ways to alleviate the adverse effects and provide new directions for the improvement of treatment strategies for diseases caused by Psn gene mutations.展开更多
Cardiovascular disease(CVD)remains the leading cause of morbidity and mortality worldwide,accounting for approximately 17.9 million deaths each year(31%of all global deaths).Cardiovascular aging(CVA)not only contribut...Cardiovascular disease(CVD)remains the leading cause of morbidity and mortality worldwide,accounting for approximately 17.9 million deaths each year(31%of all global deaths).Cardiovascular aging(CVA)not only contributes to the aging of other organ systems,leading to systemic aging in individuals,but also induces CVDs that impose serious health challenges and exacerbate CVA.Notably,non-coding RNAs(ncRNAs)such as mi RNAs,lncRNAs,and circRNAs have emerged as key players in CVA and associated CVDs(AR-CVDs)by acting as proaging,anti-aging,or dual-regulating ncRNAs.They influence both vascular aging and cardiac aging processes through modulating pro-aging or anti-aging substrates and triggers,leading to cellular senescence and CVA-related phenotypes and associated pathological processes,including hypertension,atherosclerosis,coronary heart disease,cardiac hypertrophy,heart failure,and arrhythmias.This review aims to provide an overview of the current understanding of ncRNAs in CVA and AR-CVDs,focusing on the published studies that utilize in vitro and in vivo models of aging and aging-related cardiovascular pathophysiological processes.It does not aim to exhaustively cover all ncRNA studies unrelated to aging but to present a more holistic and integrated perspective on the diverse roles of mi RNAs,lncRNAs,and circRNAs in the context of CVA and AR-CVDs.In doing so,we will explore both shared and unique aspects of ncRNAs from various angles,shedding light on their regulatory roles in CVA and AR-CVDs,which may offer insights into the current state and future directions of the field.By integrating recent findings and ongoing research,this review seeks to elucidate the intricate network of ncRNAs in CVA and AR-CVDs,paving the way for novel approaches to combat one of the most pressing health challenges of our time.展开更多
文摘Age-associated changes in cardiovascular structure/ function are implicated in the markedly increased risk for cardiovascular disease in older persons. Aging not only prolongs exposure to several other cardiovascular risks, but also leads to intrinsic cardiac changes, which reduces cardiac functional reserve, predisposes the heart to stress and contributes to increased cardiovascular mortality in the elderly. Intrinsic cardiac aging in the murine model closely recapitulates age-related cardiac changes in humans, includ- ing left ventricular hypertrophy, fibrosis and diastolic dysfunction. Cardiac aging in mice is accompanied by accumulation of mitochondrial protein oxidation, increased mitochondrial DNA mutations, increased mitochondrial biogenesis, as well as decreased cardiac SERCA2 protein. All of these age-related changes are significantly attenu- ated in mice overexpressing catalase targeted to mitochondria （mCAT）. These findings demonstrate the critical role of rnitochondrial reactive oxygen species （ROS） in cardiac ag ing and support the potential antioxidants to cardiac aging lar diseases. application of mitochondrial and age-related cardiovascular diseases.
基金supported by grants from the National Natural Science Foundation of China(81800245,81970228,82102306,81900779)the China Postdoctoral Science Foundation(2020M670030ZX)+1 种基金the Shaoguan Science and Technology Program(2019sn078)the Start-up Fund for RAPs under the Strategic Hiring Scheme(P0035913)。
文摘The literature is full of claims regarding the consumption of polyphenol or polyamine-rich foods that offer some protection from developing cardiovascular disease(CVD). This is achieved by preventing cardiac hypertrophy and protecting blood vessels through improving the function of endothelium. However, do these interventions work in the aged human hearts? Cardiac aging is accompanied by an increase in left ventricular hypertrophy, along with diastolic and systolic dysfunction. It also confers significant cardiovascular risks for both sexes. The incidence and prevalence of CVD increase sharply at an earlier age in men than women. Furthermore, the patterns of heart failure differ between sexes, as do the lifetime risk factors. Do caloric restriction(CR)-mimetics, rich in polyphenol or polyamine, delay or reverse cardiac aging equally in both men and women? This review will discuss three areas:(1) mechanisms underlying age-related cardiac remodeling;(2) gender-related differences and potential mechanisms underlying diminished cardiac response in older men and women;(3) we select a few polyphenol or polyamine rich compounds as the CRmimetics, such as resveratrol, quercetin, curcumin, epigallocatechin gallate and spermidine, due to their capability to extend health-span and induce autophagy. We outline their abilities and issues on retarding aging in animal hearts and preventing CVD in humans. We discuss the confounding factors that should be considered for developing therapeutic strategies against cardiac aging in humans.
基金This work was supported by the National Natural Science Foundation of China[Grant No.32000832]the Shandong Province Natural Science Foundation[Grant No.ZR2020QC096].
文摘Presenilin(Psn)protein is associated with organismal aging.Mutations in the Psn gene may lead to Alzheimer’s disease(AD),dilated cardiomyopathy(DCM),and many age-dependent degenerative diseases.These diseases seriously affect the quality of life and longevity of the population and place a huge burden on health care and economic systems around the world.Humans have two types of Psn,presenilin-1(PSEN1)and presenilin-2(PSEN2).Mutations in the genes encoding PSEN1,PSEN2,and amyloid precursor protein(APP)have been identified as the major genetic causes of AD.Psn is a complex gene strongly influenced by genetic and environmental factors.The effects of exercise,training,and a high-fat diet on the Psn gene expressed in the heart and its related pathways are not fully understood.Fortunately,relevant aspects of the mutational effects on Psn can be studied experimentally in easily handled animal models,including Drosophila,mice,and other animals,all of which share orthologous genes of Psn with humans.Many previous studies have linked aging,exercise training,and a high-fat diet to the Psn gene.This review discusses the interrelationship between aging,exercise training,and a high-fat diet on the Psn gene and its associated disease,AD.The aim is to understand the adverse effects of Psn gene mutations on the body and the diseases caused by AD,find ways to alleviate the adverse effects and provide new directions for the improvement of treatment strategies for diseases caused by Psn gene mutations.
基金supported by the Basic and Applied Basic Research Foundation of Guangdong Province(2022A1515220184)the Natural Science Foundation of Guangdong Province(2021A1515010547)。
文摘Cardiovascular disease(CVD)remains the leading cause of morbidity and mortality worldwide,accounting for approximately 17.9 million deaths each year(31%of all global deaths).Cardiovascular aging(CVA)not only contributes to the aging of other organ systems,leading to systemic aging in individuals,but also induces CVDs that impose serious health challenges and exacerbate CVA.Notably,non-coding RNAs(ncRNAs)such as mi RNAs,lncRNAs,and circRNAs have emerged as key players in CVA and associated CVDs(AR-CVDs)by acting as proaging,anti-aging,or dual-regulating ncRNAs.They influence both vascular aging and cardiac aging processes through modulating pro-aging or anti-aging substrates and triggers,leading to cellular senescence and CVA-related phenotypes and associated pathological processes,including hypertension,atherosclerosis,coronary heart disease,cardiac hypertrophy,heart failure,and arrhythmias.This review aims to provide an overview of the current understanding of ncRNAs in CVA and AR-CVDs,focusing on the published studies that utilize in vitro and in vivo models of aging and aging-related cardiovascular pathophysiological processes.It does not aim to exhaustively cover all ncRNA studies unrelated to aging but to present a more holistic and integrated perspective on the diverse roles of mi RNAs,lncRNAs,and circRNAs in the context of CVA and AR-CVDs.In doing so,we will explore both shared and unique aspects of ncRNAs from various angles,shedding light on their regulatory roles in CVA and AR-CVDs,which may offer insights into the current state and future directions of the field.By integrating recent findings and ongoing research,this review seeks to elucidate the intricate network of ncRNAs in CVA and AR-CVDs,paving the way for novel approaches to combat one of the most pressing health challenges of our time.
基金supported by the Shenzhen Medical Research Fund(No.D2401012)the National Natural Science Foundation of China(Nos.62275168,62275164,62204253+7 种基金82360055)the Guangdong Natural Science Foundation and Province Project(Nos.2021A1515011916 and 2023A1515012250)the Foundation from Department of Science and Technology of Guangdong Province(No.2021QN02Y124)the Foundation from Department of Education of Guangdong Province(No.2023ZDZX2052)the Medical-Engineering Interdisciplinary Research Foundation of Shenzhen University(No.2023YG002)the Scientific Instrument Developing Project of Shenzhen University(No.2023YQ008)the Shenzhen University 2035 Program for Excellent Research(Nos.2024C012 and 2024C013)the Characteristic Innovation Projects of Provincial Department of Education(No.2024KTSCX190)。
文摘Mitochondrial dynamics critically regulate cellular aging.Two-photon nonlinear structured illumination microscopy(TPSIM),a low-phototoxicity live-cell imaging technique,was employed to dynamically track mitochondrial changes in senescent H9C2 cardiomyocytes.System validation in COS7 cells achieved 82-nm resolution,threefold higher than conventional microscopy,and sustained 5-min dynamic imaging.Compared to normal cells,senescent cells exhibited fragmented mitochondria.TP-SIM further captured impaired mitochondrial fusion dynamics during senescence through continuous imaging,demonstrating its dual capability for subcellular-resolution visualization and prolonged organelle tracking in live cells.
