粒体自噬
肌发生
骨骼肌
生物
细胞生物学
线粒体
心肌细胞
生物能学
自噬
解剖
遗传学
细胞凋亡
作者
Fasih Ahmad Rahman,Joe Quadrilatero
标识
DOI:10.1016/j.semcdb.2021.11.026
摘要
Mitochondrial turnover in the form of mitophagy is emerging as a central process in maintaining cellular function. The degradation of damaged mitochondria through mitophagy is particularly important in cells/tissues that exhibit high energy demands. Skeletal muscle is one such tissue that requires precise turnover of mitochondria in several conditions in order to optimize energy production and prevent bioenergetic crisis. For instance, the formation of skeletal muscle (i.e., myogenesis) is accompanied by robust turnover of low-functioning mitochondria to eventually allow the formation of high-functioning mitochondria. In mature skeletal muscle, alterations in mitophagy-related signaling occur during exercise, aging, and various disease states. Nonetheless, several questions regarding the direct role of mitophagy in various skeletal muscle conditions remain unknown. Furthermore, given the heterogenous nature of skeletal muscle with respect to various cellular and molecular properties, and the plasticity in these properties in various conditions, the involvement and characterization of mitophagy requires more careful consideration in this tissue. Therefore, this review will highlight the known mechanisms of mitophagy in skeletal muscle, and discuss their involvement during myogenesis and various skeletal muscle conditions. This review also provides important considerations for the accurate measurement of mitophagy and interpretation of data in skeletal muscle.
科研通智能强力驱动
Strongly Powered by AbleSci AI