氧化应激
活性氧
线粒体
细胞生物学
骨骼肌
肌肉萎缩
线粒体ROS
萎缩
生物
氧化磷酸化
调解人
化学
生物化学
内分泌学
遗传学
作者
Edwin R. Miranda,Justin L. Shahtout,Katsuhiko Funai
标识
DOI:10.1089/ars.2022.0151
摘要
Significance: Accumulation of reactive oxygen species (ROS) is known to promote cellular damage in multiple cell types. In skeletal muscle, ROS has been implicated in disuse-induced muscle atrophy. However, the molecular origin and mechanism of how disuse promotes ROS and muscle dysfunction remains unclear. Recent Advances: Recently, we implicated membrane lipids of mitochondria to be a potential source of ROS to promote muscle atrophy. Critical Issues: In this review, we discuss evidence that changes in mitochondrial lipids represent a physiologically relevant process by which disuse promotes mitochondrial electron leak and oxidative stress. Future Directions: We further discuss lipid hydroperoxides as a potential downstream mediator of ROS to induce muscle atrophy. Antioxid. Redox Signal . 38, 338–351.
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