Ferroptosis in arterial atherosclerosis: mechanistic hypotheses, cell type specific vulnerabilities, translational biomarkers, and therapeutic opportunities
By
Cai Li
Jinxia Wang
Jingyi Sun
June 24, 2026
Clinical Scorecard: Ferroptosis in Atherosclerotic Arteries: Mechanistic Insights, Cell-Specific Vulnerabilities, Potential Biomarkers, and Therapeutic Avenues
At a Glance
Category Detail
Condition Atherosclerosis Key Mechanisms Ferroptosis, lipid peroxidation, oxidative stress, inflammation Target Population Patients with atherosclerosis, particularly those with diabetes, chronic kidney disease, and systemic inflammation Care Setting Clinical research and management of atherosclerosis
Key Highlights
Ferroptosis contributes to endothelial dysfunction and plaque instability. Oxidative phospholipid stress is a common feature in atherosclerotic lesions. Intermittent hyperlipidemia is a distinct driver of atherosclerosis. IL-1β primes macrophages for ferroptosis, creating a feedback loop of inflammation. Defective efferocytosis leads to necrotic core expansion in plaques. Guideline-Based Recommendations
Diagnosis
Assess oxidative stress markers and lipid profiles in patients. Management
Target iron availability and lipid peroxidation in therapeutic strategies. Monitoring & Follow-up
Evaluate biomarkers related to ferroptosis and plaque stability. Risks
Consider the implications of residual risk in patients despite lipid-lowering therapies. Patient & Prescribing Data
Individuals with atherosclerosis and associated risk factors.
Focus on therapies that modulate ferroptosis and oxidative stress.
Clinical Best Practices
Incorporate assessments of ferroptosis in the management of atherosclerosis. Monitor for signs of plaque instability in high-risk patients. Utilize targeted therapies that address lipid peroxidation and iron metabolism. Related Resources & Content
