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The autophagic degradation of BMAL1 and CLOCK, termed Clockophagy, is a recently identified pathway for ferroptosis [93], which could intersect with BD pathogenesis

Site-specific conjugation of a selenopolypeptide to alpha-1-antitrypsin enhances oxidation resistance and Pharmacological properties

Their broad protective actions highlight strong nutraceutical potential for disease prevention and treatment (74)

Additionally, supplementation with functional metabolites such as -alanine, carnosine, and acetyl-CoA (acetate) has been found to reverse EndMT, a key process in atherogenesis

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