Ferroptosis as a novel therapeutic target for cardiovascular disease

Cell death is an important component of the pathophysiology of cardiovascular disease. An understanding of how cardiomyocytes die, and why regeneration of cells in the heart is limited, is a critical area of study. Ferroptosis is a form of regulated cell death that is characterized by iron overload, leading to accumulation of lethal levels of lipid hydroperoxides. The metabolism of iron, lipids, amino acids and glutathione tightly controls the initiation and execution of ferroptosis. Emerging evidence shows that ferroptosis is closely associated with the occurrence and progression of various diseases. In recent years, ferroptosis has been found to play critical roles in cardiomyopathy, myocardial infarction, ischemia/reperfusion injury, and heart failure. This article reviews the mechanisms by which ferroptosis is initiated and controlled and discusses ferroptosis as a novel therapeutic target for various cardiovascular diseases.

Automated summary

Cell death is a significant factor in cardiovascular disease pathophysiology. Ferroptosis, a regulated cell death form characterized by iron overload and lipid hydroperoxide accumulation, is closely associated with various diseases and plays critical roles in cardiomyopathy, myocardial infarction, ischemia/reperfusion injury, and heart failure. Targeting ferroptosis may offer potential novel therapeutic strategies for cardiovascular diseases.