期刊
EXPERIMENTAL GERONTOLOGY
卷 43, 期 1, 页码 24-33出版社
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.exger.2007.10.001
关键词
skeletal; muscle; mitochondria; DNA; mutations; ROS; deletions; vicious; cycle; electron; transport; chain
资金
- NIA NIH HHS [1 P30 AG 028740, AG 17994, R01 AG017994-07, R01 AG021042-05, R01 AG021042, P30 AG028740, R01 AG017994, AG 21042] Funding Source: Medline
- NATIONAL INSTITUTE ON AGING [R01AG021042, R01AG017994, P30AG028740] Funding Source: NIH RePORTER
Aging is associated with a progressive loss of skeletal muscle mass and strength and the mechanisms mediating these effects likely involve mitochondrial DNA (mtDNA) mutations, mitochondrial dysfunction and the activation of mitochondrial-mediated apoptosis. Because the mitochondrial genome is densely packed and close to the main generator of reactive oxygen species (ROS) in the cell, the electron transport chain (ETC), an important role for mtDNA mutations in aging has been proposed. Point mutations and deletions in mtDNA accumulate with age in a wide variety of tissues in mammals, including humans, and often coincide with significant tissue dysfunction. Here, we examine the evidence supporting a causative role for mtDNA mutations in aging and sarcopenia. We review experimental outcomes showing that mtDNA mutations, leading to mitochondrial dysfunction and possibly apoptosis, are causal to the process of sarcopenia. Moreover, we critically discuss and dispute an important part of the mitochondrial 'vicious cycle' theory of aging which proposes that accumulation of mtDNA mutations may lead to an enhanced mitochondrial ROS production and ever increasing oxidative stress which ultimately leads to tissue deterioration and aging. Potential mechanism(s) by which mtDNA mutations may mediate their pathological consequences in skeletat muscle are also discussed. Published by Elsevier Inc.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据