Iron metabolism and ferroptosis in cardiovascular diseases: progress in the mechanism and pharmacological intervention.

Accumulating evidence highlights the pivotal role of ferroptosis in diverse cardiovascular diseases (CVDs) such as atherosclerosis, aortic aneurysm, aortic dissection, vascular aging, calcific aortic valve disease, myocardial ischemia reperfusion injury, cardiomyopathy, and heart failure. Studies on the molecular mechanism of ferroptosis have revealed potential targets for the treatment of CVDs, and a large number of studies have reported evidence of drug-mediated ferroptosis and iron metabolism mechanisms intervening in CVDs. This review delves into the latest molecular characteristics of ferroptosis, associated biological processes, and regulatory pathways. Notably, various compounds like iron chelators (e.g., deferoxamine, deferiprone), chloroiodohydroxyquin and its derivatives, antioxidants (e.g., vitamin E, lipoic acid, selenium), Ferrostatin-1 (Fer-1), etc., have demonstrated efficacy in animal studies against CVDs, offering cardiovascular protection. In summary, this review outlines the role of ferroptosis in CVDs, the regulatory effects of relevant drugs (including natural products) on ferroptosis within cardiovascular contexts, aiming to provide valuable insights for CVDs management and the development of novel therapeutics.