Thus, skeletal muscle atrophy, characterized by loss of muscle mass and strength, could have severe impact on daily living or even become life-threatening ( Jackman and Kandarian, 2004). Skeletal muscle carries out multiple critical functions of human body such as locomotion, metabolism, and thermogenesis ( Block, 1994 Qiu et al., 2018).
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This discovery motivated us to contribute this review article to inspire further discussion about the potential mechanisms underlying differential outcomes of physiological mitochondrial Ca 2+ transients and pathological mitochondrial Ca 2+ elevation in skeletal muscle ROS production. Interestingly, a recent study has revealed an unexpected role of rapid mitochondrial Ca 2+ transients in keeping mPTP at a closed state with reduced mitochondrial ROS production. There are various mechanistic studies that focus on the excitation-transcription coupling framework to understand the beneficial role of exercise and electrical stimulation. Meanwhile, electrical stimulation is known to help prevent apoptosis and alleviate muscle atrophy in denervated animal models and patients with motor impairment. Previously, both acute and long-term endurance exercises have been reported to activate certain signaling pathways to counteract ROS production. However, the outcomes of this steady-state elevation of mitochondrial Ca 2+ level include exacerbated reactive oxygen species (ROS) generation, sensitized opening of mitochondrial permeability transition pore (mPTP), induction of programmed cell death, and ultimately muscle atrophy. Pathophysiological conditions such as skeletal muscle denervation or unloading also lead to elevated Ca 2+ levels inside mitochondria. During muscle contraction, Ca 2+ influx into mitochondria activates multiple enzymes related to tricarboxylic acid (TCA) cycle and oxidative phosphorylation, resulting in increased ATP synthesis to meet the energy demand. Ca 2+ plays a multifaceted role in mitochondrial function. Mitochondria are both the primary provider of ATP and the pivotal regulator of cell death, which are essential for physiological muscle activities. Department of Kinesiology, College of Nursing and Health Innovation, The University of Texas at Arlington, Arlington, TX, United States.Ang Li *, Jianxun Yi, Xuejun Li and Jingsong Zhou *
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