Mitochondrial reactive oxygen species regulate cellular signaling and dictate biological outcomes

被引:772
作者
Hamanaka, Robert B. [1 ]
Chandel, Navdeep S. [1 ,2 ]
机构
[1] Northwestern Univ, Dept Med, Div Pulm & Crit Care Med, Sch Med, Chicago, IL 60611 USA
[2] Northwestern Univ, Sch Med, Dept Cell & Mol Biol, Chicago, IL 60611 USA
关键词
MANGANESE SUPEROXIDE-DISMUTASE; TUMOR-NECROSIS-FACTOR; COMPLEX-III; LIFE-SPAN; OXIDATIVE STRESS; REVERSIBLE OXIDATION; JNK ACTIVATION; BETA-CAROTENE; DNA-DAMAGE; HYPOXIA;
D O I
10.1016/j.tibs.2010.04.002
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
Reactive oxygen species (ROS) have historically been viewed as toxic metabolic byproducts and causal agents in a myriad of human pathologies. More recent work, however, indicates that ROS are critical intermediates of cellular signaling pathways. Although it is clear that dedicated cellular ROS producers such as NADPH oxidases participate in signaling, evidence suggests that mitochondrial production of ROS is also a tightly controlled process, and plays a role in the maintenance of cellular oxidative homeostasis and propagation of cellular signaling pathways. Production of ROS at mitochondria thus integrates cellular energy state, metabolite concentrations, and other upstream signaling events and has important implications in cellular stress signaling, maintenance of stem cell populations, cellular survival, and oncogenic transformation.
引用
收藏
页码:505 / 513
页数:9
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