Open AccessMitochondrial Quality Control in Sarcopenia: Updated Overview of Mechanisms and Interventions
Author(s) -
Di Liu,
Yu Fan,
Xiaohua Tao,
Weili Pan,
Yuxiang Wu,
Xiuhua Wang,
Yiqing He,
Wenfeng Xiao,
Yusheng Li
Publication year - 2021
Publication title -
aging and disease
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.808
H-Index - 54
ISSN - 2152-5250
DOI - 10.14336/ad.2021.0427
Subject(s) - sarcopenia , proteostasis , mitochondrial biogenesis , medicine , skeletal muscle , mitophagy , psychological intervention , autophagy , quality of life (healthcare) , ageing , mitochondrion , bioinformatics , biology , microbiology and biotechnology , psychiatry , biochemistry , apoptosis , nursing
Sarcopenia is a common geriatric disorder characterized by decreased muscle strength, low muscle mass and poor physical performance. This aging-related skeletal muscle deterioration leads to adverse outcomes and severely impairs the quality of life of patients. The accumulation of dysfunctional mitochondria with aging is an important factor in the occurrence and progression of sarcopenia. Mitochondrial quality control (MQC) fundamentally ensures the normal mitochondrial functions and is comprised of four main parts: proteostasis, biogenesis, dynamics and autophagy. Therefore, any pathophysiologic factors compromising the quality control of homeostasis in the skeletal muscle may lead to sarcopenia. However, the specific theoretical aspects of these processes have not been fully elucidated. Current therapeutic interventions using nutritional and pharmaceutical treatments show a modest therapeutic efficacy; however, only physical exercise is recommended as the first-line therapy for sarcopenia, which can ameliorate skeletal muscle deficiency by maintaining the homeostatic MQC. In this review, we summarized the known mechanisms that contribute to the pathogenesis of sarcopenia by impairing normal mitochondrial functions and described potential interventions that mitigate sarcopenia through improving MQC.