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Under oxidative stress, excessive Ca 2+ influx into mitochondria exacerbates mPTP activation and ΔΨm loss ( 2+ dysregulation converge to drive mitochondrial collapse, ATP depletion, and skeletal myocyte apoptosis or necrosis-ultimately contributing to the pathogenesis of muscle atrophy ( 5.2.2 Mitochondrial dysfunction exacerbates ROS production: a vicious cycle Mitochondrial dysfunction both amplifies ROS generation and impairs antioxidant defense, establishing a self-perpetuating cycle of oxidative injury and organelle deterioration ( Mitophagy serves as a key quality control mechanism that selectively eliminates dysfunctional mitochondria, thereby limiting ROS accumulation and preserving metabolic homeostasis ( In chronic ischemic conditions-such as rotator cuff tears-HIF-1α/BNIP3 signaling is disrupted, leading to impaired mitophagy homeostasis and persistent mitochondrial stress