粒体自噬
线粒体融合
骨骼肌
细胞生物学
生物
线粒体
内科学
功能(生物学)
内分泌学
线粒体分裂
线粒体生物发生
医学
自噬
生物化学
线粒体DNA
基因
细胞凋亡
作者
Chantal A. Pileggi,Gaganvir Parmar,Mary‐Ellen Harper
摘要
Summary Skeletal muscle possesses dramatic metabolic plasticity that allows for the rapid adaptation in cellular energy transduction to meet the demands of the organism. Obesity elicits changes in skeletal muscle structure and function, resulting in the accumulation of intramuscular lipids. The accumulation of intramuscular lipids in obesity is associated with impaired skeletal muscle mitochondrial content and function. Mitochondria exist as a dynamic network that is regulated by the processes of biogenesis, fusion, fission, and mitophagy. In this review, we outline adaptations in molecular pathways that regulate mitochondrial structure and function in obesity. We highlight the emerging role of dysregulated skeletal muscle macroautophagy and mitochondrial turnover in obesity. Future research should further elucidate the role of mitophagy in observed reductions in mitochondrial content and function during obesity.
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