Review discusses fiber-type-specific mechanisms mitigating muscle atrophy in conditions like type-2 diabetes, indicating potential drug targets.
Skeletal muscle is essential for life as it enables physical movement, maintains posture, is crucial for breathing, and serves as a major site for energy and carbohydrate metabolism. Pathological conditions that reduce skeletal muscle mass and function—such as muscular dystrophies, motor‐neuron diseases, cancer, type‐2 diabetes, or aging—have detrimental effects on human health, reducing quality of life and survival. Currently, exercise is the only validated treatment for increasing muscle mass and function, but it is impractical for bedridden patients or the frail elderly. Significant advances in understanding the molecular mechanisms underlying atrophy of slow‐ or fast‐twitch muscle fibers have identified numerous previously unknown key players that may show promise as potential drug targets. Here, we review these recent advances and discuss the potential of these discovered mechanisms as therapeutic targets to combat muscle wasting.
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Chakraborty et al. (2025) studied this question.