Journal
CELLULAR AND MOLECULAR LIFE SCIENCES
Volume 78, Issue 4, Pages 1305-1328Publisher
SPRINGER BASEL AG
DOI: 10.1007/s00018-020-03662-0
Keywords
Atrophy; Mitochondria; Fission; Fusion; Mitochondrial proteostasis; Autophagy; Mitophagy; Skeletal muscle; FGF21; Myokines
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Funding
- Universita degli Studi di Padova within the CRUI-CARE Agreement
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Maintaining the function of mitochondria in skeletal muscle requires dynamic coordination of processes controlling mitochondrial network quality, which in turn affects muscle mass and performance. Loss of muscle mass increases the risk of disease onset and premature death, with exercise being the best approach to improve mitochondrial health and slow atrophy in various diseases.
The dynamic coordination of processes controlling the quality of the mitochondrial network is crucial to maintain the function of mitochondria in skeletal muscle. Changes of mitochondrial proteolytic system, dynamics (fusion/fission), and mitophagy induce pathways that affect muscle mass and performance. When muscle mass is lost, the risk of disease onset and premature death is dramatically increased. For instance, poor quality of muscles correlates with the onset progression of several age-related disorders such as diabetes, obesity, cancer, and aging sarcopenia. To date, there are no drug therapies to reverse muscle loss, and exercise remains the best approach to improve mitochondrial health and to slow atrophy in several diseases. This review will describe the principal mechanisms that control mitochondrial quality and the pathways that link mitochondrial dysfunction to muscle mass regulation.
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