IGF1 is a growth factor with pleiotropic effects on skeletal muscle development, bone metabolism, and metabolic homeostasis. Primary mechanism: IGF1 binds IGF1R, activating intrinsic tyrosine kinase activity and downstream PI3K-AKT and Ras-MAPK signaling cascades [UniProt]. In skeletal muscle, IGF1 promotes myotube differentiation toward a mature oxidative phenotype with enhanced contractility, myofibril assembly, mitochondrial respiration, and glucose uptake via GLUT4 upregulation 1. Beyond myogenesis, IGF1 suppression has emerged as a disease target: in androgenetic alopecia, AR-promoted miR-221 suppresses IGF1, inactivating MAPK/PI3K-AKT pathways in hair follicle cells 2. In osteoarthritis, Wnt signaling-induced IGF1 transcription drives joint damage; cartilage-specific Igf1 deletion protects against post-traumatic disease 3. IGF1 also exhibits neuroprotective properties: microglia-derived IGF1 promotes GABAergic neurogenesis in prenatal human brain 4, and TREM2-IGF1 signaling reprograms microglia toward a neuroprotective phenotype during ischemic stroke, restoring glucometabolic function 5. Clinically, excessive IGF1 characterizes acromegaly, where prolonged hormone elevation causes systemic manifestations and increased mortality, requiring surgical, radiotherapeutic, or pharmacological intervention 6. IGF1 deficiency is an associated disease state, while excessive signaling requires therapeutic suppression in certain pathologies.