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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.

The study demonstrated that MT-DADMe-ImmA, a potent inhibitor of MTAP, effectively induced apoptosis in head and neck cancer cell lines FaDu and Cal27 by increasing MTA levels and decreasing polyamines, leading to mitochondrial changes and activation of caspases. This treatment selectively targeted cancer cells without affecting normal fibroblasts, suggesting its potential as a cancer treatment. In a mouse model, MT-DADMe-ImmA led to tumor remission, highlighting its promise for cancers sensitive to DNA methylation changes. Despite inducing apoptosis, the treatment did not alter the protein levels of mitochondrial markers Bcl2 and Bax.