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作 者:Hai Bo Ning Jiang Li Li Ji Yong Zhang
机构地区:[1]Tianjin Key Laboratory of Exercise Physiology and Sports Medicine,Department of Health & Exercise Science,Tianjin University of Sport [2]Department of Military Training Medicines,Logistics University of Chinese People's Armed Police Force [3]Laboratory of Physiological Hygiene and Exercise Science,School of Kinesiology,University of Minnesota
出 处:《Journal of Sport and Health Science》2013年第2期67-74,共8页运动与健康科学(英文)
基 金:supported by research grants from the National Natural Science Foundation of China(No.31110103919, 31200894,31000523,30771048,30470837,31071040,and 30270638);Tianjin Municipal Sci-tech-innovation Base Project (No.10SYSYJC28400);Tianjin Science and Technology Planning Project(No.12JCQNJC07900);General Administration of Sport of China Basic Project(No.10B058)
摘 要:Mitochondrial redox metabolism has long been recognized as being central to the effects of aging and the development of age-related pathologies in the major oxidative organs. Consistent evidence has shown that exercise is able to retard the onset and impede the progression of aging by modifying mitochondrial oxidant--antioxidant homeostasis. Here we provide a broad overview of the research evidence showing the relationship between mitochondrial redox metabolism, aging and exercise. We address part aspects of mitochondrial reactive oxygen species (ROS) metabolism, from superoxide production to ROS detoxification, especially antioxidant enzymes and uncoupling protein. Furthermore, we describe mitochondrial remodeling response to aging and exercise, which is accompanied by bioenergetics and redox regulation. In addition, potential mechanisms for redox signaling involved in mitochondrial remodeling and redox metabolism regulation are also reviewed.线粒体氧化还原长久以来被认为对衰老及主要氧化器官中年龄相关的疾病发生有重要影响。现有证据一致表明,运动能通过改变线粒体氧化—抗氧化内平衡来延缓发病、阻碍衰老。本文就线粒体氧化还原代谢、衰老与运动之间的关系进行广泛的研究证据文献综述。其中包括线粒体活性氧(ROS)代谢方面,从超氧化物产生到ROS解毒,特别是抗氧化酶及解偶联蛋白。本文还描述了伴有生物能和氧化还原调节的针对衰老和运动的线粒体重构反应。最后,本文回顾了参与线粒体重构和氧化还原代谢调节的氧化还原信号的潜在机制。
关 键 词:AGING EXERCISE Mitochondrial remodeling PGC-1Α Reactive oxygen species
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