Circadian Clock in Muscle Disease Etiology and Therapeutic Potential for Duchenne Muscular Dystrophy

被引:2
作者
Kiperman, Tali [1 ]
Ma, Ke [1 ]
机构
[1] Beckman Res Inst City Hope, Arthur Riggs Diabet & Metab Res Inst, Dept Diabet Complicat & Metab, Duarte, CA 91010 USA
关键词
circadian clock; muscle regeneration; myogenesis; satellite cells; muscular dystrophy; small molecule; drug development; MDX MOUSE MODEL; ARNT-LIKE; REV-ERB; NUCLEAR RECEPTORS; SATELLITE CELL; GENE-THERAPY; IN-VIVO; MOLECULAR REGULATION; SLEEP-DEPRIVATION; ELBOW FLEXORS;
D O I
10.3390/ijms25094767
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Circadian clock and clock-controlled output pathways exert temporal control in diverse aspects of skeletal muscle physiology, including the maintenance of muscle mass, structure, function, and metabolism. They have emerged as significant players in understanding muscle disease etiology and potential therapeutic avenues, particularly in Duchenne muscular dystrophy (DMD). This review examines the intricate interplay between circadian rhythms and muscle physiology, highlighting how disruptions of circadian regulation may contribute to muscle pathophysiology and the specific mechanisms linking circadian clock dysregulation with DMD. Moreover, we discuss recent advancements in chronobiological research that have shed light on the circadian control of muscle function and its relevance to DMD. Understanding clock output pathways involved in muscle mass and function offers novel insights into the pathogenesis of DMD and unveils promising avenues for therapeutic interventions. We further explore potential chronotherapeutic strategies targeting the circadian clock to ameliorate muscle degeneration which may inform drug development efforts for muscular dystrophy.
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页数:21
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