Oxidative stress, mitochondrial dysfunction, and aging.

Journal of signal transduction Pub Date : 2012-01-01 Epub Date: 2011-10-02 DOI:10.1155/2012/646354
Hang Cui, Yahui Kong, Hong Zhang
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引用次数: 831

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.

氧化应激,线粒体功能障碍和衰老。
衰老是一种复杂的现象,其特征是生理功能的逐渐衰退和死亡率的增加,并常伴有许多病理性疾病。尽管衰老在所有生物体中几乎是普遍保守的,但衰老的潜在分子机制在很大程度上仍然是难以捉摸的。人们提出了许多关于衰老的理论,包括自由基和线粒体衰老理论。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产生增强,进一步损伤mtDNA。在本文中,我们将介绍ROS和线粒体之间相互作用的当前理解,并将讨论它们对衰老和年龄相关疾病的潜在影响。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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