MitoQ Upregulates CYP19A1 to Protect Dermal Papilla Cells from DHT-Induced Mitochondrial Dysfunction and Apoptosis in Androgenetic Alopecia

The study investigates the role of MitoQ, a mitochondria-targeted antioxidant, in protecting dermal papilla cells (DPCs) from dihydrotestosterone (DHT)-induced mitochondrial dysfunction and apoptosis in androgenetic alopecia (AGA). It highlights that MitoQ upregulates CYP19A1 (aromatase), which converts androgens into estrogens, thereby sustaining mitochondrial homeostasis under androgenic stress. The research used a DHT-induced AGA mouse model and DPCs with manipulated CYP19A1 expression to demonstrate that both CYP19A1 and MitoQ reduce mitochondrial reactive oxygen species, improve respiratory capacity, and preserve mitochondrial morphology. These findings suggest that the CYP19A1–mitochondrial axis could be a promising target for AGA treatment, as it reveals a novel aromatase–mitochondria cross-talk in hair-follicle cells.