Nrf2 mediates redox adaptations to exercise

被引:225
作者
Done, Aaron J. [1 ]
Traustadottir, Tinna [1 ]
机构
[1] No Arizona Univ, Dept Biol Sci, Flagstaff, AZ 86011 USA
关键词
Acute exercise; Regular exercise; Phase II enzymes; Reactive oxygen species; Cell signaling; NFE2L2; HO-1; SOD; OXIDATIVE STRESS; ANTIOXIDANT RESPONSE; SKELETAL-MUSCLE; MODERATE EXERCISE; RECEPTOR FUNCTION; VITAMIN-C; MECHANISMS; EXPRESSION; SYSTEM; SUPPLEMENTATION;
D O I
10.1016/j.redox.2016.10.003
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
070307 [化学生物学]; 071010 [生物化学与分子生物学];
摘要
The primary aim of this review is to summarize the current literature on the effects of acute exercise and regular exercise on nuclear factor erythroid 2-related factor 2 (Nrf2) activity and downstream targets of Nrf2 signaling. Nrf2 (encoded in humans by the NFE2L2 gene) is the master regulator of antioxidant defenses, a transcription factor that regulates expression of more than 200 cytoprotective genes. Increasing evidence indicates that Nrf2 signaling plays a key role in how oxidative stress mediates the beneficial effects of exercise. Episodic increases in oxidative stress induced through bouts of acute exercise stimulate Nrf2 activation and when applied repeatedly, as with regular exercise, leads to upregulation of endogenous antioxidant defenses and overall greater ability to counteract the damaging effects of oxidative stress. The evidence of Nrf2 activation in response to exercise across variety of tissues may be an important mechanism of how exercise exerts its well-known systemic effects that are not limited to skeletal muscle and myocardium. Additionally there are emerging data that results from animal studies translate to humans.
引用
收藏
页码:191 / 199
页数:9
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