Ferroptosis mechanisms and regulations in cardiovascular diseases in the past, present, and future

Cardiovascular diseases (CVDs) are the main diseases that endanger human health, and their risk factors contribute to high morbidity and a high rate of hospitalization. Cell death is the most important pathophysiology in CVDs. As one of the cell death mechanisms, ferroptosis is a new form of regulated cell death (RCD) that broadly participates in CVDs (such as myocardial infarction, heart transplantation, atherosclerosis, heart failure, ischaemia/reperfusion (I/R) injury, atrial fibrillation, cardiomyopathy (radiation-induced cardiomyopathy, diabetes cardiomyopathy, sepsis-induced cardiac injury, doxorubicin-induced cardiac injury, iron overload cardiomyopathy, and hypertrophic cardiomyopathy), and pulmonary arterial hypertension), involving in iron regulation, metabolic mechanism and lipid peroxidation. This article reviews recent research on the mechanism and regulation of ferroptosis and its relationship with the occurrence and treatment of CVDs, aiming to provide new ideas and treatment targets for the clinical diagnosis and treatment of CVDs by clarifying the latest progress in CVDs research. • The identification, development history and characterization of ferroptosis. • The role of different subcellular organelles and organelle-specific regulators in ferroptosis. • The mechanism of ferroptosis includes iron metabolism, amino acid metabolism, and lipid metabolism. • The role of ferroptosis in different cardiovascular cells and cardiovascular diseases. • The treatment efficacy and pathological mechanism involved in ferroptosis and cardiovascular diseases.