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线粒体与生物寿命。

Mitochondria and organismal longevity.

机构信息

Division of Molecular and Life Science, Pohang University of Science and Technology, Pohang, Kyungbuk, South Korea.

出版信息

Curr Genomics. 2012 Nov;13(7):519-32. doi: 10.2174/138920212803251427.

Abstract

Mitochondria are essential for various biological processes including cellular energy production. The oxidative stress theory of aging proposes that mitochondria play key roles in aging by generating reactive oxygen species (ROS), which indiscriminately damage macromolecules and lead to an age-dependent decline in biological function. However, recent studies show that increased levels of ROS or inhibition of mitochondrial function can actually delay aging and increase lifespan. The aim of this review is to summarize recent findings regarding the role of mitochondria in organismal aging processes. We will discuss how mitochondria contribute to evolutionarily conserved longevity pathways, including mild inhibition of respiration, dietary restriction, and target of rapamycin (TOR) signaling.

摘要

线粒体对于各种生物过程至关重要,包括细胞能量产生。衰老的氧化应激理论提出,线粒体通过产生自由基(ROS)在衰老中发挥关键作用,自由基会无差别地破坏大分子,并导致生物功能随年龄的增长而下降。然而,最近的研究表明,ROS 水平的增加或线粒体功能的抑制实际上可以延缓衰老并延长寿命。本综述的目的是总结线粒体在机体衰老过程中的作用的最新发现。我们将讨论线粒体如何促进包括呼吸轻度抑制、饮食限制和雷帕霉素靶蛋白(TOR)信号在内的进化保守的长寿途径。

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