It is well-accepted that oxidative stress and inflammation play key roles in the pathogenesis of various cardiovascular disorders including atherosclerosis heart failure, ischemia/reperfusion injury and stroke, and the physiologic process of aging.

Here, we provide an overview of the features, process, function, and mechanisms of ferroptosis, and its increasingly connected relevance to oxidative stress, inflammation, and cardiovascular diseases.Д¬ardiovascular diseases (CVDs) are the leading causes of morbidity and mortality worldwide. Accumulating evidence suggests that ferroptosis is implicated in a variety of cardiovascular diseases such as atherosclerosis, stroke, ischemia-reperfusion injury, and heart failure, indicating that targeting ferroptosis will present a novel therapeutic approach against cardiovascular diseases. Ferroptosis plays an important role in the regulation of oxidative stress and inflammatory responses. Iron metabolism and lipid peroxidation signaling are increasingly recognized as central mediators of ferroptosis. The dysfunction of lipid peroxide clearance, the presence of redox-active iron as well as oxidation of polyunsaturated fatty acid (PUFA)-containing phospholipids are three essential features of ferroptosis.

This form of cell death does not exhibit typical morphological and biochemical characteristics, including cell shrinkage, mitochondrial fragmentation, nuclear condensation. Ferroptosis, a recently identified and iron-dependent cell death, differs from other cell death such as apoptosis, necroptosis, pyroptosis, and autophagy-dependent cell death.

R hearts of iron