Physiological Roles of Mitochondrial Reactive Oxygen Species

被引：2033

作者：

Sena, Laura A. ^{[1
]}

Chandel, Navdeep S. ^{[1
,2
]}

机构：

[1] Northwestern Univ, Dept Med, Feinberg Sch Med, Div Pulm & Crit Care Med, Chicago, IL 60611 USA

[2] Northwestern Univ, Dept Cell & Mol Biol, Feinberg Sch Med, Chicago, IL 60611 USA

来源：

MOLECULAR CELL | 2012年 / 48卷 / 02期

关键词：

HYPOXIC PULMONARY VASOCONSTRICTION; ACTIVATED CALCIUM-CHANNELS; CHRONOLOGICAL LIFE-SPAN; COMPLEX-III; UNCOUPLING PROTEIN-2; ROS PRODUCTION; STEM-CELLS; INFLAMMASOME ACTIVATION; INDUCED TRANSCRIPTION; ANTIOXIDANT ENZYMES;

D O I：

10.1016/j.molcel.2012.09.025

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：

Historically, mitochondrial reactive oxygen species (mROS) were thought to exclusively cause cellular damage and lack a physiological function. Accumulation of ROS and oxidative damage have been linked to multiple pathologies, including neurodegenerative diseases, diabetes, cancer, and premature aging. Thus, mROS were originally envisioned as a necessary evil of oxidative metabolism, a product of an imperfect system. Yet few biological systems possess such flagrant imperfections, thanks to the persistent optimization of evolution, and it appears that oxidative metabolism is no different. More and more evidence suggests that mROS are critical for healthy cell function. In this Review, we discuss this evidence following some background on the generation and regulation of mROS.

引用

页码：158 / 167

页数：10

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