Scholarlink

Abstract <p>Progressive age-related decline in skeletal muscle mass, strength,and function results in muscle fiber loss and atrophy, with associatedreplacement by adipose and fibrous tissue, or sarcopenia. Musclesare liable to multiple forms of molecular and cellular damage, includingimpaired regenerative capacity and protein turnover, mitochondrialdysfunction, and cellular senescence, which manifests as cell cycle arrest.With age, these cells accumulate and acquire distinctive propertiescharacterized by chromatin changes and the emergence of a specificsecretory senescence-associated phenotype (SAS phenotype), whichexerts local and/or systemic negative effects on tissues. The aimof this review is to present the landscape of cellular senescencein skeletal muscle, based on the evidence for their role in age-related changesin muscle mass, strength, function, and clinical consequences ofthis phenomenon, as well as to outline key directions in developingnovel anti-senescence therapies for sarcopenia. Data search was carriedout in Google Scholar, Medline, PubMed, Scopus, Web of Science,and Cochrane Library electronic scientific databases using keywordsand their combinations, with the AMSTAR 2 software. Publicationselection (82 included out of 430) was performed randomly, followedby independent assessment of their methodological quality. The crucialrole of cellular senescence in shaping the SAS phenotype in theage-related pathophysiology of skeletal muscles has been proven.These phenomena alter muscle tissue homeostasis and contribute tothe onset and progression of sarcopenia. Targeting senescent cellsand their secretory profiles may facilitate the development of complexstrategies, including the use of senolytics and senomorphics, toimprove the quality of life in aging human populations. On the otherhand, there are currently insufficient data on the vulnerabilityto aging of terminally differentiated skeletal muscle fibers andresident mononuclear cells in the interstitial microenvironment.A range of opinions is discussied on how this phenomenon contributesto the onset and progression of age-related skeletal muscle lossand dysfunction, as well as the initiation of sarcopenia. Scientificadvancements in this field will enable the identification of noveltherapeutic approaches to optimizing muscle health in old age.</p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

Cellular Senescence in Skeletal Muscle: Age, Sarcopenia, Therapy

  • 期刊论文

  • 发表日期：

    2025年5月1日

查看全文
  • N. G. Plekhova,
  • P. A. Novikova,
  • A. N. Voro,
  • D. V. Korolev,
  • V. B. Shumatov

摘要

Abstract

Progressive age-related decline in skeletal muscle mass, strength,and function results in muscle fiber loss and atrophy, with associatedreplacement by adipose and fibrous tissue, or sarcopenia. Musclesare liable to multiple forms of molecular and cellular damage, includingimpaired regenerative capacity and protein turnover, mitochondrialdysfunction, and cellular senescence, which manifests as cell cycle arrest.With age, these cells accumulate and acquire distinctive propertiescharacterized by chromatin changes and the emergence of a specificsecretory senescence-associated phenotype (SAS phenotype), whichexerts local and/or systemic negative effects on tissues. The aimof this review is to present the landscape of cellular senescencein skeletal muscle, based on the evidence for their role in age-related changesin muscle mass, strength, function, and clinical consequences ofthis phenomenon, as well as to outline key directions in developingnovel anti-senescence therapies for sarcopenia. Data search was carriedout in Google Scholar, Medline, PubMed, Scopus, Web of Science,and Cochrane Library electronic scientific databases using keywordsand their combinations, with the AMSTAR 2 software. Publicationselection (82 included out of 430) was performed randomly, followedby independent assessment of their methodological quality. The crucialrole of cellular senescence in shaping the SAS phenotype in theage-related pathophysiology of skeletal muscles has been proven.These phenomena alter muscle tissue homeostasis and contribute tothe onset and progression of sarcopenia. Targeting senescent cellsand their secretory profiles may facilitate the development of complexstrategies, including the use of senolytics and senomorphics, toimprove the quality of life in aging human populations. On the otherhand, there are currently insufficient data on the vulnerabilityto aging of terminally differentiated skeletal muscle fibers andresident mononuclear cells in the interstitial microenvironment.A range of opinions is discussied on how this phenomenon contributesto the onset and progression of age-related skeletal muscle lossand dysfunction, as well as the initiation of sarcopenia. Scientificadvancements in this field will enable the identification of noveltherapeutic approaches to optimizing muscle health in old age.