有氧运动调控线粒体质量控制改善心肌肥厚的研究进展

贾 浩1 , 宋寅平1 , 滑艺杰1 , 李贯文2 , 马 美1 , 陈 伟1 , 王友华1,*
1陕西师范大学体育学院,西安 710119 2西北民族大学体育学院,兰州 730000

摘 要:

心肌肥厚是对各种生物力学和病理性刺激引起心脏工作需求增加的一种代偿。研究表明,线粒体在心肌肥厚发生发展过程中扮演重要角色,线粒体动力学紊乱、线粒体自噬不足及线粒体生物发生减弱进一步恶化心肌肥厚为心力衰竭。有氧运动作为有效改善心肌肥厚的非药物干预手段,在调控线粒体质量控制,改善线粒体分裂、融合、自噬等方面发挥重要作用,可有效抑制心肌肥厚的病理发展。该文综述了近年来心肌肥厚发生发展的分子机制及其研究进展,进一步论述了有氧运动对其改善的分子机制,拟为预防和治疗心肌肥厚提供新的思路和理论依据。

通讯作者:王友华 , Email:wangyouh@snnu.edu.cn

Research progress of myocardial hypertrophy improvement by aerobic exercise-regulated mitochondrial quality control
JIA Hao1 , SONG Yin-Ping1 , HUA Yi-Jie1 , LI Guan-Wen2 , MA Mei1 , CHEN Wei1 , WANG You-Hua1,*
1Department of Physical Education, Shaanxi Normal University, Xi’an 710119, China 2Department of Physical Education, Northwest University for Nationalities, Lanzhou 730000, China

Abstract:

Cardiac hypertrophy is a compensation for the increased demands of heart work output caused by various biomechanical and pathophysiological stimuli. Studies have shown that mitochondria play an important role
in the occurrence and development of cardiac hypertrophy. Mitochondrial kinetic disorders, insufficient mitochondrial autophagy, and weakened mitochondrial biogenesis make cardiac hypertrophy further develop into heart failure. Aerobic exercise as a non-pharmacological intervention to effectively improve cardiac hypertrophy can inhibit the pathological development of cardiac hypertrophy by regulating mitochondrial quality control, improving mitochondrial division, fusion, autophagy, etc. This article reviews the molecular mechanism and research progress of cardiac hypertrophy in recent years, and further discusses the molecular mechanisms of improving cardiac function by aerobic exercise, and intends to provide new ideas and theoretical basis for the prevention and treatment of cardiac hypertrophy.

Communication Author:WANG You-Hua , Email:wangyouh@snnu.edu.cn

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