Ferroptosis: the potential value target in atherosclerosis

Area of Science:

• Cardiovascular Biology
• Cell Death Mechanisms
• Atherosclerosis Pathogenesis

Background:

• Advanced atherosclerosis is characterized by necrotic cores and vulnerable plaques due to defective cell death.
• Ferroptosis, a novel iron-dependent cell death, is implicated in promoting atherosclerosis via oxidative damage and endothelial dysfunction.
• Disordered intracellular iron metabolism contributes to cellular damage and exacerbates AS risk factors like inflammation and dyslipidemia.

Purpose of the Study:

• To elucidate the role and mechanisms of ferroptosis in the development and progression of atherosclerosis.
• To explore the correlation between ferroptosis and various pathological processes in AS.
• To establish a theoretical foundation for future research into ferroptosis-driven atherosclerosis.

Main Methods:

• Literature review of recent findings on cell death mechanisms in atherosclerosis.
• Analysis of studies investigating ferroptosis, iron metabolism, and their impact on vascular cells.
• Synthesis of current knowledge on the links between ferroptosis and AS pathogenesis.

Main Results:

• Ferroptosis accelerates atherosclerosis by promoting lipid peroxidation and endothelial dysfunction.
• Impaired iron homeostasis in ferroptosis damages macrophages, VSMCs, and VECs.
• Ferroptosis is linked to key AS pathological processes including oxidative stress, inflammation, and dyslipidemia.

Conclusions:

• Ferroptosis is a significant contributor to atherosclerosis development and progression.
• Further investigation into ferroptosis mechanisms is essential for understanding AS.
• This review provides a theoretical basis for future therapeutic strategies targeting ferroptosis in AS.