心力衰竭患者运动不耐受的骨骼肌线粒体机制研究进展
Advances in mitochondrial mechanisms of skeletal muscle for exercise intolerance in heart failure patients
随着人口老龄化进程心力衰竭的发病率和死亡率不断上升,已成为我国面临的重要公共卫生问题。而严重的运动不耐受是心力衰竭患者的主要临床表现之一,严重影响生活质量。越来越多的证据表明,外周功能障碍,尤其是骨骼肌功能障碍,是导致心力衰竭患者运动不耐受的重要原因,而不仅是通常认为的心脏原因。值得注意的是线粒体结构和功能障碍在骨骼肌功能障碍中占主导地位。目前针对心力衰竭运动不耐受的治疗方法中,有氧运动是唯一且循证医学证据级别最高的基础疗法。该文围绕线粒体的生物合成、融合与裂解以及自噬分析了引起心力衰竭患者骨骼肌功能障碍进而导致运动不耐受的机制,并进一步讨论了运动训练可否通过改善骨骼肌线粒体功能改善心力衰竭患者的运动耐受性。
更多Severe exercise intolerance is one of the main clinical manifestations in heart failure (HF) patients, which seriously affects patients′ quality of life. Recent studies have demonstrated that peripheral dysfunction, especially the skeletal muscle dysfunction, is a fundamental cause of exercise intolerance, rather than conventionally perceived cardiac factors. Notably, the alternation of mitochondrial function and structure dominate skeletal muscle dysfunction, and aerobic exercise is the only basic treatment for HF patients with the highest level of evidence-based medicine. This article reviews research advances on the mechanisms of skeletal muscle dysfunction and exercise intolerance in HF patients, focusing on the biogenesis, fusion, fission and autophagy of mitochondria, and further discusses the possibility of exercise training for enhancing exercise tolerance through improving mitochondrial function in HF patients.
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