Sarcopenia is a progressive and multifactorial muscle disorder associated with diminished strength, reduced functional capacity, and increased risk of adverse health outcomes including frailty, falls, and mortality. Despite its clinical burden, the molecular pathogenesis of sarcopenia remains poorly understood, which hinders the development of precise therapeutic strategies. This review examines emerging evidence linking anabolic resistance, mitochondrial dysfunction, neuromuscular instability, and chronic inflammation to impaired regeneration and disrupted proteostasis. While nutritional interventions such as high-quality protein, leucine metabolites, and vitamin D supplementation preserve lean mass, they fail to consistently restore function independently. Although exercise remains the cornerstone therapy, its benefits are often constrained in patients with multimorbidity or reduced mobility. Given the biological heterogeneity of sarcopenia, there is a need to shift from generic supportive care to stratified, mechanism-based therapy. Emerging omics technologies including transcriptomic, proteomic, and metabolic profiling offer a promising avenue to define molecular endotypes. This will guide the development of precision-based management strategies.
Chin et al. (Sun,) studied this question.