Human umbilical cord-derived mesenchymal stem cells ameliorate muscle dysfunction and metabolic dysregulation in the CuZnSOD null mouse model of sarcopenia

muscle, particularly omega-3 fatty acids, which was selectively rescued by UC-MSC therapy, including restoration of α-linolenic acid, eicosapentaenoic acid, and docosahexaenoic acid, without substantial recovery of disrupted polar metabolic pathways such as aminoacyl-tRNA biosynthesis. In contrast, UC-MSC administration in wild-type mice induced a distinct metabolic remodeling characterized by reduced n-3 and n-6 fatty acid-associated lipid species and concomitant enrichment of fructose-related glycolytic intermediates, indicating a shift toward carbohydrate-based energy utilization in metabolically intact muscle. Together, these findings demonstrate that UC-MSCs function as context-dependent metabolic modulators, alleviating oxidative stress-induced sarcopenia through attenuation of oxidative stress, restoration of systemic IGF-1, and selective reprogramming of lipid metabolism, while dynamically adjusting energy metabolism in physiological skeletal muscle.