Utilizing zebrafish models to elucidate mechanisms and develop therapies for skeletal muscle atrophy

Abstract

Skeletal muscle atrophy, resulting from an imbalance in muscle protein synthesis and degradation, compromises muscle quality and function, imposing significant burdens on movement and metabolic stability. Animal models are crucial for understanding the mechanisms of skeletal muscle atrophy and developing clinical prevention and treatment strategies. Zebrafish, as small aquatic vertebrates, exhibit high genetic homology with humans and offer advantages such as rapid reproduction, development, and transparent embryos. Their physiological and anatomical similarities to mammals, including a substantial proportion of skeletal muscle and observable swimming behavior reflecting body dysfunction, make zebrafish an ideal model for studying skeletal muscle-related diseases. This review outlines the development of zebrafish skeletal muscle and highlights key pathways regulating muscle proteins, emphasizing their anatomical and genetic consistency with humans. Various zebrafish models of skeletal muscle atrophy created through physical, chemical, and gene-editing methods are systematically summarized. Current challenges and proposed improvement strategies are also discussed to enhance the reliability and applicability of zebrafish models, providing a comprehensive reference for advancing research on skeletal muscle atrophy.