Mustn1 in Skeletal Muscle: A Novel Regulator?

被引:2
作者
Kim, Charles J. [1 ,2 ]
Hadjiargyrou, Michael [1 ,2 ]
机构
[1] New York Inst Technol, Coll Osteopath Med, Old Westbury, NY 11568 USA
[2] New York Inst Technol, Dept Biol & Chem Sci, Old Westbury, NY 11568 USA
关键词
Mustn1; skeletal muscle; development; repair; knockout; mouse; MUSCULAR-DYSTROPHY; SATELLITE CELLS; GENE; EXPRESSION; IDENTIFICATION; FIBROBLASTS; MYOBLASTS; PROMOTER; DISEASES; FAMILIES;
D O I
10.3390/genes15070829
中图分类号
Q3 [遗传学];
学科分类号
071007 ; 090102 ;
摘要
Skeletal muscle is a complex organ essential for locomotion, posture, and metabolic health. This review explores our current knowledge of Mustn1, particularly in the development and function of skeletal muscle. Mustn1 expression originates from Pax7-positive satellite cells in skeletal muscle, peaks during around the third postnatal month, and is crucial for muscle fiber differentiation, fusion, growth, and regeneration. Clinically, Mustn1 expression is potentially linked to muscle-wasting conditions such as muscular dystrophies. Studies have illustrated that Mustn1 responds dynamically to injury and exercise. Notably, ablation of Mustn1 in skeletal muscle affects a broad spectrum of physiological aspects, including glucose metabolism, grip strength, gait, peak contractile strength, and myofiber composition. This review summarizes our current knowledge of Mustn1's role in skeletal muscle and proposes future research directions, with a goal of elucidating the molecular function of this regulatory gene.
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页数:20
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