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氧化应激、线粒体功能障碍与衰老。

Oxidative stress, mitochondrial dysfunction, and aging.

作者信息

Cui Hang, Kong Yahui, Zhang Hong

机构信息

Department of Cell Biology, University of Massachusetts Medical School, Worcester, MA 01655, USA.

出版信息

J Signal Transduct. 2012;2012:646354. doi: 10.1155/2012/646354. Epub 2011 Oct 2.

Abstract

Aging is an intricate phenomenon characterized by progressive decline in physiological functions and increase in mortality that is often accompanied by many pathological diseases. Although aging is almost universally conserved among all organisms, the underlying molecular mechanisms of aging remain largely elusive. Many theories of aging have been proposed, including the free-radical and mitochondrial theories of aging. Both theories speculate that cumulative damage to mitochondria and mitochondrial DNA (mtDNA) caused by reactive oxygen species (ROS) is one of the causes of aging. Oxidative damage affects replication and transcription of mtDNA and results in a decline in mitochondrial function which in turn leads to enhanced ROS production and further damage to mtDNA. In this paper, we will present the current understanding of the interplay between ROS and mitochondria and will discuss their potential impact on aging and age-related diseases.

摘要

衰老 是一种复杂的现象,其特征是生理功能逐渐衰退,死亡率上升,且常常伴有多种病理疾病。尽管衰老在所有生物中几乎普遍存在,但其潜在的分子机制仍 largely难以捉摸。已经提出了许多衰老理论,包括自由基衰老理论和线粒体衰老理论。这两种理论都推测,活性氧(ROS)对线粒体和线粒体DNA(mtDNA)的累积损伤是衰老的原因之一。氧化损伤影响mtDNA的复制和转录,导致线粒体功能下降,进而导致ROS产生增加,并进一步损伤mtDNA。在本文中,我们将阐述目前对ROS与线粒体之间相互作用的理解,并讨论它们对衰老和与年龄相关疾病的潜在影响。

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