Signalling Pathways in Striated Muscle Differentiation, Histogenesis and Repair

Dear Colleagues,

This Special Issue aims to bring together recent and current research associated with signaling pathways regulating striated muscle differentiation, histogenesis, and remodeling. This is a re-edition of a previous issue published in 2020, but with a broader focus on both skeletal and cardiac (striated) muscle, taking into account the fact that both tissues undergo changes in response to similar physiological or pathological stimuli. Indeed, both muscles are dynamic tissues capable of responding to a large variety of stimuli by adjusting muscle growth, size, metabolism, and function. Numerous recent studies have expanded our knowledge of the complexity of the signaling pathways regulating these processes. Indeed, it is becoming clear that a precisely regulated process, involving endocrine/paracrine and cell–cell contact interactions, is required for the maintenance of muscle homeostasis. Alterations of these mechanisms lead to unsuccessful repair in response to direct mechanical trauma (acute injury) or following secondary damage because of aging or genetic defects. Striated muscle biology is studied from many different viewpoints: genetic diseases, sports medicine, physiology, immunology, developmental biology, gene regulation, and regeneration. In recent years, advances in our understanding of the mechanisms of muscle diseases and disfunctions have led to a major focus on translational research and pharmacological therapies for clinically important muscle pathologies. The focus of this Special Issue is to bring together studies that use different experimental approaches in vivo or in vitro to dissect the dynamic changes taking place in muscle building and maintenance, and their contribution to normal versus pathological muscle repair. 

Prof. Dr. Marina Bouché
Dr. Biliana Lozanoska-Ochser
Guest Editors

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• signaling pathways
• skeletal muscle
• cardiac muscle
• muscle development
• muscle homeostasis
• muscle atrophy
• muscular dystrophies
• satellite cells
• tissue regeneration
• inflammation