Exercise, mitochondrial dysfunction and inflammasomes in skeletal muscle

被引:8
|
作者
Slavin, Mikhaela B. [1 ]
Khemraj, Priyanka [1 ]
Hood, David A. [1 ,2 ]
机构
[1] York Univ, Muscle Hlth Res Ctr, Sch Kinesiol & Hlth Sci, Toronto, ON M3J 1P3, Canada
[2] York Univ, Sch Kinesiol & Hlth Sci, 4700 Keele St, Toronto, ON M3J 1P3, Canada
基金
加拿大自然科学与工程研究理事会;
关键词
Mitochondria; Skeletal muscle; Aging; Muscle disuse; Exercise; Inflammation; NF-KAPPA-B; NLRP3; INFLAMMASOME; STRENUOUS EXERCISE; IN-VITRO; ACTIVATION; EXPRESSION; MECHANISMS; INCREASES; DAMAGE; INFILTRATION;
D O I
10.1016/j.bj.2023.100636
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
In the broad field of inflammation, skeletal muscle is a tissue that is understudied. Yet it represents about 40% of body mass in non-obese individuals and is therefore of fundamental importance for whole body metabolism and health. This article provides an overview of the unique features of skeletal muscle tissue, as well as its adaptability to exercise. This ability to adapt, particularly with respect to mitochondrial content and function, confers a level of metabolic "protection" against energy consuming events, and adds a measure of quality control that determines the phenotypic response to stress. Thus, we describe the particular role of mitochondria in promoting inflammasome activation in skeletal muscle, contributing to muscle wasting and dysfunction in aging, disuse and metabolic disease. We will then discuss how exercise training can be anti-inflammatory, mitigating the chronic inflammation that is observed in these conditions, potentially through improvements in mitochondrial quality and function.
引用
收藏
页数:8
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