Molecular Mechanisms and Targeted Therapeutics in Androgenetic Alopecia: From Signaling Pathways to Regenerative Approaches

Androgenetic alopecia (AGA) is the most common type of hair loss in both sexes, marked by progressive follicular shrinking influenced by genetic, hormonal, metabolic, and environmental variables. This study offers an extensive examination of AGA, addressing its epidemiology, hair biology, pathophysiology, and both existing and emerging treatment modalities. Androgenetic alopecia (AGA) is significantly affected by androgens, especially dihydrotestosterone (DHT), which engages androgen receptors and modifies local growth factor signaling, resulting in hair follicle regression. Genetic susceptibility, disruptions in signaling pathways (WNT/β-catenin, BMP, FGF5), hormonal abnormalities, dietary inadequacies, environmental exposures, and inflammation collectively contribute to the illness. Presently, FDA-sanctioned treatments comprise topical minoxidil and oral finasteride, but novel therapies emphasize stem cell interventions, JAK inhibitors, WNT pathway activators, prostaglandin analogs, and innovative biologics aimed at the molecular causes underlying follicle shrinking. Non-pharmacological therapies, including platelet-rich plasma, microneedling, low-level laser therapy, and hair transplantation, offer supplementary therapeutic advantages. Comprehending the multifaceted etiology of AGA is essential for formulating individualized and efficient treatment options.