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Increases SIRT-1 activity as a result of enhanced NAD+ salvage, leading to beneficial epigenetic and metabolic reprogramming, including increased oxidative phosphorylation (OXPHOS) and muscle stem cell activation 1-3

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(72) demonstrated, using a rat left coronary artery ligation model, that vitexin reduced MDA levels in cardiomyocytes while increasing SOD and NADPH activities, thereby inhibiting lipid peroxidation, preventing cardiomyocyte ferroptosis, and improving cardiac function

To investigate whether these theoretical hunches had any real-world basis, Raz and Lu approached Bechhoefer, an experimentalist