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Aging compromises the brains metabolic efficiency, primarily due to mitochondrial dysfunction and cumulative oxidative damage to mtDNA (Scharf et al., 2008)

The clinical and biochemical features of diclofenac hepatotoxicity in humans and rats relates both to impairment of ATP synthesis by mitochondria, and to production of active metabolites, particularly N,5- dihydroxydiclofenac, which causes direct cytotoxicity

This mechanism overlaps with how minoxidil benefits follicles, though via a distinct route: minoxidil widens existing vessels, whereas VEGF upregulation promotes the formation of new ones

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