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This study demonstrates that MitoQ can alleviate symptoms of androgenetic alopecia (AGA) by targeting mitochondrial dysfunction and enhancing CYP19A1 expression, which regulates the WNT/β-catenin signaling pathway. In a mouse model of DHT-induced hair loss, MitoQ was shown to reverse hair growth reduction and mitigate apoptosis caused by decreased CYP19A1 expression. Network pharmacology identified 75 drug targets and 367 disease targets, highlighting MitoQ's potential in hormonal response and transcriptional regulation pathways. These findings suggest that MitoQ could be a promising therapeutic intervention for AGA, with CYP19A1 as a valuable target.

This case report described a six-year-old boy with congenital generalized hypertrichosis terminalis, a rare condition characterized by excessive growth of pigmented terminal hair, gingival hyperplasia, and a coarse face. The boy, born to non-consanguineous parents, also had congenital hydronephrosis and a heterozygous deletion on chromosome 17q12. Despite normal intellectual development, he exhibited shyness and dependency on his mother. Laboratory tests showed normal results, and a right-sided nephrectomy was performed due to severe hydronephrosis. The report highlighted the need for regular follow-ups with endocrinologists and nephrologists due to potential risks of diabetes mellitus and renal issues. Laser hair removal was initiated and proved effective. The study suggested a possible genetic link involving chromosome 17q but noted that a specific molecular abnormality had not been identified.