Oxidative stress, mitochondrial dysfunction, and aging.
Oxidative stress, mitochondrial dysfunction, and aging.
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DOI：
10.1155/2012/646354
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发表时间：
2012
期刊：
影响因子：
--
通讯作者：
Zhang H
中科院分区：
文献类型：
--
作者：
Cui H;Kong Y;Zhang H
衰老是一个复杂的现象，其特征是生理功能的逐渐下降和死亡率的增加，往往伴随着许多病理性疾病。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难以捉摸。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。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。氧化损伤影响线粒体DNA的复制和转录，导致线粒体功能下降，这反过来又导致ROS产生增加，进一步损伤线粒体DNA。在本文中，我们将介绍目前对ROS和线粒体之间相互作用的理解，并将讨论它们对衰老和年龄相关疾病的潜在影响。
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.