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Moreover, cardiomyocyte-specific knockdown of HADHA exacerbated cardiac dysfunction in mice, whereas treatment with Fer-1, an inhibitor of ferroptosis, effectively rescued cardiac function, supporting the conclusion that HADHA deficiency promotes ferroptosis predominantly through reactive oxygen species accumulation and glutathione depletion

It has the capacity to be able to pass through all biological membranes due to its small molecular size and high lipophilicity and it is evenly distributed to all biological tissues and fluids by crossing the bloodbrain barrier [3]

Atherosclerosis as pathogenetic substrate for Sars-Cov 2 cytokine storm

Methods 228 , 6778 (2014)