首页> 外文期刊>The Journal of Physiology >Mitochondria in the middle: exercise preconditioning protection of striated muscle
【24h】

Mitochondria in the middle: exercise preconditioning protection of striated muscle

机译:中间的线粒体:运动预处理保护横纹肌

获取原文
获取原文并翻译 | 示例
           

摘要

Cellular and physiological adaptations to an atmosphere which became enriched in molecular oxygen spurred the development of a layered system of stress protection, including antioxidant and stress response proteins. At physiological levels reactive oxygen and nitrogen species regulate cell signalling as well as intracellular and intercellular communication. Exercise and physical activity confer a variety of stressors on skeletal muscle and the cardiovascular system: mechanical, metabolic, oxidative. Transient increases of stressors during acute bouts of exercise or exercise training stimulate enhancement of cellular stress protection against future insults of oxidative, metabolic and mechanical stressors that could induce injury or disease. This phenomenon has been termed both hormesis and exercise preconditioning (EPC). EPC stimulates transcription factors such as Nrf-1 and heat shock factor-1 and up-regulates gene expression of a cadre of cytosolic (e.g. glutathione peroxidase and heat shock proteins) and mitochondrial adaptive or stress proteins (e.g. manganese superoxide dismutase, mitochondrial K-ATP channels and peroxisome proliferator activated receptor coactivator-1 (PGC-1)). Stress response and antioxidant enzyme inducibility with exercise lead to protection against striated muscle damage, oxidative stress and injury. EPC may indeed provide significant clinical protection against ischaemia-reperfusion injury, Type II diabetes and ageing. New molecular mechanisms of protection, such as -opioid receptor regulation and mitophagy, reinforce the notion that mitochondrial adaptations (e.g. heat shock proteins, antioxidant enzymes and sirtuin-1/PGC-1 signalling) are central to the protective effects of exercise preconditioning.
机译:细胞和生理对大气中富含分子氧的适应性促进了压力保护分层系统的发展,包括抗氧化剂和压力响应蛋白。在生理水平,活性氧和氮物质调节细胞信号传导以及细胞内和细胞间通讯。运动和体育锻炼会在骨骼肌和心血管系统上产生各种压力源:机械的,代谢的,氧化的。在急性运动或运动训练过程中,应激源的短暂增加刺激了细胞应激保护作用的增强,以抵抗将来可能引起伤害或疾病的氧化,代谢和机械应激源的损害。这种现象已被称为兴奋剂和运动预处理(EPC)。 EPC刺激转录因子,例如Nrf-1和热休克因子-1,并上调细胞溶质(例如谷胱甘肽过氧化物酶和热休克蛋白)和线粒体适应性或应激蛋白(例如锰超氧化物歧化酶,线粒体K- ATP通道和过氧化物酶体增殖物激活的受体coactivator-1(PGC-1)。运动引起的压力反应和抗氧化酶诱导作用可防止横纹肌损伤,氧化应激和损伤。 EPC确实可以为缺血再灌注损伤,II型糖尿病和衰老提供重要的临床保护。新的保护性分子机制,例如-阿片受体调节和线粒体吞噬,增强了线粒体适应性(例如热休克蛋白,抗氧化酶和sirtuin-1 / PGC-1信号传导)对运动预处理的保护作用至关重要的观念。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱:kefu@zhangqiaokeyan.com

京公网安备:11010802029741号 ICP备案号:京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有
  • 客服微信

  • 服务号