Research progress on the role of ferroptosis in cardiovascular disease

Area of Science:

• Molecular Biology
• Cardiovascular Medicine
• Cell Death Pathways

Background:

• Cardiovascular diseases (CVDs) are complex and pose significant health risks.
• Cardiomyocyte death is a key factor in CVD development.
• Ferroptosis, distinct from apoptosis, autophagy, and pyroptosis, is increasingly recognized in CVD pathogenesis.

Purpose of the Study:

• To systematically review the molecular mechanisms of ferroptosis in various cardiovascular diseases.
• To delineate the regulatory network connecting ferroptosis and cardiovascular diseases.
• To highlight potential therapeutic targets for inhibiting ferroptosis in CVD treatment.

Main Methods:

• Systematic literature review focusing on ferroptosis mechanisms in cardiovascular contexts.
• Analysis of regulatory pathways involving lipid, amino acid, and iron metabolism in ferroptosis.
• Identification and summary of potential therapeutic interventions, including small molecules and genetic approaches.

Main Results:

• Ferroptosis, driven by lipid peroxidation and iron overload, is implicated in arrhythmia, atherosclerosis, and myocardial ischemia/reperfusion.
• Lipid, amino acid, and iron metabolism are critical regulators of the ferroptosis pathway.
• Small molecule compounds (iron chelators, antioxidants, ferroptosis inhibitors) and genetic interventions show potential in mitigating CVD by targeting ferroptosis.

Conclusions:

• Ferroptosis plays a pivotal role in the occurrence and progression of diverse cardiovascular diseases.
• Targeting and inhibiting ferroptosis in cardiomyocytes represents a feasible and promising therapeutic strategy for cardiovascular diseases.
• Understanding the ferroptosis regulatory network is key to developing novel treatments for CVD.