Chicken or Egg? Mitochondrial Phospholipids and Oxidative Stress in Disuse-Induced Skeletal Muscle Atrophy

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. Recently, we implicated membrane lipids of mitochondria to be a potential source of ROS to promote muscle atrophy. 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. We further discuss lipid hydroperoxides as a potential downstream mediator of ROS to induce muscle atrophy. Antioxid. Redox Signal. 38, 338-351.