Mitochondrial dysfunction in aging: Much progress but many unresolved questions

被引：260

作者：

Payne, Brendan A. I. ^{[1
]}

Chinnery, Patrick F. ^{[1
]}

机构：

[1] Newcastle Univ, Inst Med Genet, Wellcome Trust Ctr Mitochondrial Res, Newcastle Upon Tyne NE1 7RU, Tyne & Wear, England

来源：

BIOCHIMICA ET BIOPHYSICA ACTA-BIOENERGETICS | 2015年 / 1847卷 / 11期

基金：

英国惠康基金; 英国医学研究理事会;

关键词：

DNA; Mitochondrial; Aging; SKELETAL-MUSCLE MITOCHONDRIAL; CYTOCHROME-C-OXIDASE; MTDNA CONTROL-REGION; AGE-RELATED-CHANGES; DNA MUTATIONS; LIFE-SPAN; PHYSICAL-ACTIVITY; OXIDATIVE DAMAGE; POINT MUTATIONS; CALORIE RESTRICTION;

D O I：

10.1016/j.bbabio.2015.05.022

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

The free radical theory of aging is almost 60 years old. As mitochondria are the principle source of intracellular reactive oxygen species (ROS), this hypothesis suggested a central role for the mitochondrion in normal mammalian aging. In recent years, however, much work has questioned the importance of mitochondrial ROS in driving aging. Conversely new evidence points to other facets of mitochondrial dysfunction which may nevertheless suggest the mitochondrion retains a critical role at the center of a complex web of processes leading to cellular and organismal aging. Crown Copyright (c) 2015 Published by Elsevier B.V.

引用

页码：1347 / 1353

页数：7

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