Abstract
Both iron overload and deficiency can promote development of cardiomyopathy. Advances in our knowledge from recent research have indicated numerous potential cellular mechanisms. Regulation of myocardial autophagy by iron is of particular interest and will be reviewed here. Autophagy is already well established to play a significant role in regulating the development of heart failure. This review will focus on regulation of autophagy by iron, crosstalk between autophagy and other cellular process which have also already been implicated in heart failure (oxidative stress, mitochondrial dysfunction, endoplasmic reticulum stress, ferroptosis) and the therapeutic potential of targeting these interactions.