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Conclusion Cysteine metabolism plays a crucial role in the pathogenesis of AA, impacting diverse biological pathways ranging from oxidative stress and disturbances in keratin functionality to autophagy, immunity and ferroptosis

Hyperhomocysteinemia may worsen PD neuropathology and related neuroinflammation by activating the NF-B and NLRP3 inflammasome signaling pathways

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These senescent cells linger in tissues and continuously secrete a toxic cocktail of pro-inflammatory cytokines, driving systemic inflammation

However, many of these compounds have extremely long half-lives (the rate of elimination of a substance), often measured in years

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