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运动对线粒体缺陷治疗作用的分子基础

Molecular Basis for the Therapeutic Effects of Exercise on Mitochondrial Defects.

作者信息

Memme Jonathan M, Hood David A

机构信息

Muscle Health Research Centre, York University, Toronto, ON, Canada.

School of Kinesiology and Health Science, York University, Toronto, ON, Canada.

出版信息

Front Physiol. 2021 Jan 13;11:615038. doi: 10.3389/fphys.2020.615038. eCollection 2020.

DOI:10.3389/fphys.2020.615038
PMID:33584337
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7874077/
Abstract

Mitochondrial dysfunction is common to many organ system disorders, including skeletal muscle. Aging muscle and diseases of muscle are often accompanied by defective mitochondrial ATP production. This manuscript will focus on the pre-clinical evidence supporting the use of regular exercise to improve defective mitochondrial metabolism and function in skeletal muscle, through the stimulation of mitochondrial turnover. Examples from aging muscle, muscle-specific mutations and cancer cachexia will be discussed. We will also examine the effects of exercise on the important mitochondrial regulators PGC-1α, and Parkin, and summarize the effects of exercise to reverse mitochondrial dysfunction (e.g., ROS production, apoptotic susceptibility, cardiolipin synthesis) in muscle pathology. This paper will illustrate the breadth and benefits of exercise to serve as "mitochondrial medicine" with age and disease.

摘要

线粒体功能障碍在包括骨骼肌在内的许多器官系统疾病中都很常见。衰老的肌肉和肌肉疾病常常伴随着线粒体ATP生成缺陷。本手稿将聚焦于临床前证据,这些证据支持通过刺激线粒体更新,利用规律运动来改善骨骼肌中存在缺陷的线粒体代谢和功能。将讨论衰老肌肉、肌肉特异性突变和癌症恶病质的相关例子。我们还将研究运动对重要的线粒体调节因子PGC-1α和帕金森蛋白的影响,并总结运动在肌肉病理学中逆转线粒体功能障碍(如活性氧生成、凋亡易感性、心磷脂合成)的作用。本文将阐述运动作为“线粒体药物”在应对衰老和疾病方面的广度及益处。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/374d/7874077/f16cb9583adb/fphys-11-615038-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/374d/7874077/f16cb9583adb/fphys-11-615038-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/374d/7874077/f16cb9583adb/fphys-11-615038-g001.jpg

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Derangements of amino acids in cachectic skeletal muscle are caused by mitochondrial dysfunction.恶病质骨骼肌中氨基酸的紊乱是由线粒体功能障碍引起的。
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Exercise and mitochondrial health.运动与线粒体健康。
Cross-Species Studies Reveal That Dysregulated Mitochondrial Gene Expression and Electron Transport Complex I Activity Are Crucial for Sarcopenia.
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