Molecular mechanisms in exercise-induced cardioprotection.
Molecular mechanisms in exercise-induced cardioprotection.
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DOI：
10.4061/2011/972807
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发表时间：
2011-03-06
影响因子：
2.1
通讯作者：
Laher I
中科院分区：
文献类型：
--
作者：
Golbidi S;Laher I
缺乏身体活动越来越被认为是心血管疾病的可改变的行为危险因素。运动引起的心脏保护的拟议机制的部分列表包括热休克蛋白的诱导、心脏抗氧化能力的增加、内质网应激蛋白的表达、冠状动脉的解剖和生理变化、一氧化氮产生的变化、心脏线粒体的适应性变化、自噬增加以及肌膜和/或线粒体ATP敏感钾通道的功能改善。目前尚不清楚哪些保护机制对于运动引起的心脏保护至关重要。然而，大多数研究都集中在肌膜 KATP 通道、NO 产生和线粒体变化上，尽管很可能还存在其他机制。本文讨论了有关上述主题的当前信息，但没有考虑血液或自主神经系统内潜在的重要适应。更好地了解运动引起的心脏保护的分子基础将有助于制定更好的治疗策略。
Physical inactivity is increasingly recognized as modifiable behavioral risk factor for cardiovascular diseases. A partial list of proposed mechanisms for exercise-induced cardioprotection include induction of heat shock proteins, increase in cardiac antioxidant capacity, expression of endoplasmic reticulum stress proteins, anatomical and physiological changes in the coronary arteries, changes in nitric oxide production, adaptational changes in cardiac mitochondria, increased autophagy, and improved function of sarcolemmal and/or mitochondrial ATP-sensitive potassium channels. It is currently unclear which of these protective mechanisms are essential for exercise-induced cardioprotection. However, most investigations focus on sarcolemmal KATP channels, NO production, and mitochondrial changes although it is very likely that other mechanisms may also exist. This paper discusses current information about these aforementioned topics and does not consider potentially important adaptations within blood or the autonomic nervous system. A better understanding of the molecular basis of exercise-induced cardioprotection will help to develop better therapeutic strategies.