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肌肉减少症中的线粒体损伤

Mitochondrial Impairment in Sarcopenia.

作者信息

Bellanti Francesco, Lo Buglio Aurelio, Vendemiale Gianluigi

机构信息

Department of Medical and Surgical Sciences, University of Foggia, viale Pinto 1, 71122 Foggia, Italy.

出版信息

Biology (Basel). 2021 Jan 6;10(1):31. doi: 10.3390/biology10010031.

DOI:10.3390/biology10010031
PMID:33418869
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7825073/
Abstract

Sarcopenia is defined by the age-related loss of skeletal muscle quality, which relies on mitochondrial homeostasis. During aging, several mitochondrial features such as bioenergetics, dynamics, biogenesis, and selective autophagy (mitophagy) are altered and impinge on protein homeostasis, resulting in loss of muscle mass and function. Thus, mitochondrial dysfunction contributes significantly to the complex pathogenesis of sarcopenia, and mitochondria are indicated as potential targets to prevent and treat this age-related condition. After a concise presentation of the age-related modifications in skeletal muscle quality and mitochondrial homeostasis, the present review summarizes the most relevant findings related to mitochondrial alterations in sarcopenia.

摘要

肌肉减少症的定义是与年龄相关的骨骼肌质量丧失,这依赖于线粒体稳态。在衰老过程中,生物能量学、动力学、生物发生和选择性自噬(线粒体自噬)等几种线粒体特征会发生改变,并影响蛋白质稳态,导致肌肉质量和功能丧失。因此,线粒体功能障碍在肌肉减少症的复杂发病机制中起重要作用,线粒体被认为是预防和治疗这种与年龄相关病症的潜在靶点。在简要介绍了与年龄相关的骨骼肌质量和线粒体稳态变化后,本综述总结了与肌肉减少症中线粒体改变相关的最相关研究结果。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eaae/7825073/f38baaa223f9/biology-10-00031-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eaae/7825073/58d21e33797b/biology-10-00031-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eaae/7825073/75829361d97f/biology-10-00031-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eaae/7825073/f38baaa223f9/biology-10-00031-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eaae/7825073/58d21e33797b/biology-10-00031-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eaae/7825073/75829361d97f/biology-10-00031-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eaae/7825073/f38baaa223f9/biology-10-00031-g003.jpg

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