ACOD1 Deficiency Promotes DDX1 Methylation-Mediated Mitochondrial Dysfunction And Dermal Papilla Cell Senescence In Androgenetic Alopecia

The study investigates the role of ACOD1 deficiency in androgenetic alopecia (AGA), revealing that it promotes DDX1 methylation, leading to mitochondrial dysfunction and dermal papilla cell (DPC) senescence. Using human scalp tissues, primary DPCs, and a DHT-induced AGA mouse model, researchers found that ACOD1 knockdown resulted in increased senescence markers, mitochondrial fragmentation, and impaired cell functions. Conversely, ACOD1 overexpression and 4-octyl itaconate (4-OI) supplementation ameliorated these effects, suggesting ACOD1 as a potential therapeutic target for AGA. The findings highlight the significance of ACOD1 in maintaining mitochondrial function and preventing DPC senescence, offering insights into new treatment avenues for hair loss.