Ferroptosis and cardiovascular disease: role of free radical-induced lipid peroxidation

Area of Science:

• Cardiovascular medicine
• Cell biology
• Pathology

Background:

• Cardiovascular disease (CVD) is a leading global cause of death, primarily due to myocardial infarction from atherosclerotic plaque rupture.
• Atherosclerosis involves plaque buildup from oxidized lipids, restricting blood flow.
• Lipid peroxidation (LPO), the oxidation of polyunsaturated fatty acids, is a key factor in atherosclerosis, driving immune responses and cell death.

Purpose of the Study:

• To review recent advancements in understanding ferroptosis in cardiovascular disease (CVD) and atherosclerosis.
• To highlight the critical role of free radical lipid peroxidation (LPO) in these processes.
• To discuss the evidence for ferroptosis in CVD and identify current challenges in the field.

Main Methods:

• Literature review of recent research on ferroptosis, CVD, and atherosclerosis.
• Analysis of the role of lipid peroxidation in the pathogenesis of atherosclerosis and CVD.
• Critical discussion of the evidence linking ferroptosis to cardiovascular conditions.

Main Results:

• Ferroptosis, a novel form of regulated cell death driven by iron-dependent lipid peroxidation, is emerging as a significant contributor to CVD.
• Distinct from apoptosis and necrosis, ferroptosis involves the accumulation of lethal levels of lipid hydroperoxides.
• Evidence suggests ferroptosis plays a role in the cellular mechanisms underlying atherosclerosis and other cardiovascular diseases.

Conclusions:

• Ferroptosis is a critical cellular process implicated in the development and progression of cardiovascular disease.
• Understanding the mechanisms of ferroptosis and its link to lipid peroxidation is crucial for developing new therapeutic strategies for CVD.
• Further research is needed to fully elucidate the role of ferroptosis in CVD and address existing challenges in the field.