Mechanism of Ferroptosis: A Potential Target for Cardiovascular Diseases Treatment

Ferroptosis is a form of programmed cell death caused by production of reactive oxygen species and disequilibrium of iron homeostasis. Many chemical compounds and clinical drugs induce ferroptosis in normal and cancer cells, while peroxidation inhibitors, iron chelators, and antioxidants can block ferroptosis. Glutathione peroxidase 4, ferroptosis suppressor protein 1, nuclear factor erythroid 2-related factor 2, and system Xc(-) are the negative regulators of ferroptosis, whereas nicotinamide adenine dinucleotide phosphate oxidase, p53, mitochondria voltage-dependent anion channel, and cysteinyl-tRNA synthetase function as positive regulators. Ferroptosis plays important roles in pathogen infection and tumor immunology. Recent studies suggest that ferroptosis plays a vital role in the pathogenesis of cardiovascular diseases (CVDs), which seriously threaten human health. Potential therapies designed around ferroptosis may alter the pathological progression of CVDs. Therefore, we redacted an overview of the discovery of ferroptosis, its regulatory mechanisms, and its potential impact on CVDs treatment.

Automated summary

Ferroptosis is a form of programmed cell death triggered by oxidative stress and iron dysregulation, with various proteins and molecules playing regulatory roles. It is involved in pathogen infection, tumor immunology, and cardiovascular diseases, suggesting its potential as a therapeutic target for CVDs.