粒体自噬
溶酶体
细胞生物学
生物发生
线粒体
自噬
线粒体生物发生
细胞器生物发生
骨骼肌
自噬体
生物
生物化学
化学
内分泌学
酶
基因
细胞凋亡
作者
Matthew Triolo,David A. Hood
标识
DOI:10.1016/j.abb.2018.11.004
摘要
Skeletal muscle mitochondria are essential in providing the energy required for locomotion. In response to contractile activity, the production of mitochondria is upregulated to meet the energy demands placed upon muscle cells. In a coordinated fashion, exercise also promotes the breakdown of dysfunctional mitochondria via mitophagy. Mitophagy is characterized by the selection of poorly functioning organelles, engulfment in an autophagosome and transport to lysosomes for degradation. In addition to the activation of mitophagy, exercise also elevates lysosome biogenesis. This coordinated increase in mitophagy targeting and lysosomal biogenesis serves to enhance the capacity for autophagosomal degradation, thereby aiding in the maintenance of mitochondrial quality. Lysosome dysfunction, as observed in lysosomal storage disorders (LSDs), negatively impacts mitochondrial function likely through the suppression of mitophagy. Since exercise is capable of activating mitophagy and lysosome biogenesis, researchers have begun to investigate physical activity as an effective therapy for LSDs. This review summarizes the current understanding of how mitophagy and lysosomal biogenesis are regulated in exercising skeletal, with potential therapeutic implications.
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