Advances in research on cell models for skeletal muscle atrophy

Skeletal muscle, the largest organ in the human body, plays a crucial role in supporting and defending the body and is essential for movement. It also participates in regulating the processes of protein synthesis and degradation. Inhibition of protein synthesis and activation of degradation metabolism can both lead to the development of skeletal muscle atrophy, a pathological condition characterized by a decrease in muscle mass and fiber size. Many physiological and pathological conditions can cause a decline in muscle mass, but the underlying mechanisms of its pathogenesis remain incompletely understood, and the selection of treatment strategies and efficacy evaluations vary. Moreover, the early symptoms of this condition are often not apparent, making it easily overlooked in clinical practice. Therefore, it is necessary to develop and use cell models to understand the etiology and influencing factors of skeletal muscle atrophy. In this review, we summarize the methods used to construct skeletal muscle cell models, including hormone, inflammation, cachexia, genetic engineering, drug, and physicochemical models. We also analyze, compare, and evaluate the various construction and assessment methods. [Display omitted] •A summary of the current muscle atrophy cell models is provided to offer more assistance in studying muscle atrophy.•This paper highlights four cell models for skeletal muscle atrophy: C2C12, L6, primary cells and iPSCs.•We discuss factors including hormones, inflammatory factors, cachexia, drugs, genes, and physical-chemical factors.•Understanding these cell models helps grasp muscle atrophy and guides the construction of new experimental models.