An emerging double‑edged sword role of ferroptosis in cardiovascular disease (Review)

Area of Science:

• Biomedical Science
• Cardiovascular Research
• Cell Death Mechanisms

Background:

• Cardiovascular disease (CVD) pathogenesis involves complex mechanisms, with cardiomyocyte loss playing a critical role.
• Programmed cell death pathways, including apoptosis, autophagy, pyroptosis, and ferroptosis, are implicated in CVD progression.
• Ferroptosis, characterized by iron accumulation and lipid peroxidation, is increasingly recognized for its contribution to CVD.

Purpose of the Study:

• To provide an in-depth analysis of the mechanisms underlying ferroptosis.
• To summarize the interplay between ferroptosis and cardiovascular diseases (CVDs).
• To discuss potential therapeutic targets and future directions for ferroptosis-targeted CVD treatments.

Main Methods:

• Review of current literature on ferroptosis pathways.
• Analysis of the role of lipid, amino acid, and iron metabolism in ferroptosis.
• Examination of key ferroptosis characteristics: iron homeostasis, lipid peroxidation, glutathione levels, and glutathione peroxidase 4 activity.

Main Results:

• Ferroptosis is driven by oxidized lipids and excess iron, disrupting cellular homeostasis.
• Inhibition of ferroptosis in cardiomyocytes presents a potential therapeutic strategy for CVD.
• Ferroptosis exhibits dual roles in the pathogenesis of various CVDs.

Conclusions:

• Understanding ferroptosis mechanisms is crucial for developing novel CVD therapies.
• Targeting ferroptosis pathways offers promising preventive and therapeutic approaches for CVD.
• Further research into ferroptosis inhibitors and their clinical applications is warranted for future CVD treatment.