Current progress of ferroptosis in cardiovascular diseases

Abstract

Ferroptosis, a newly recognized form of nonapoptotic regulated cell death, is characterized by iron-dependent lipid peroxidation. Biological processes, such as iron metabolism, lipid peroxidation, and amino acid metabolism, are involved in the process of ferroptosis. However, the related molecular mechanism of ferroptosis has not yet been completely clarified, and specific and sensitive biomarkers for ferroptosis need to be explored. Recently, studies have revealed that ferroptosis probably causes or exacerbates the progress of cardiovascular diseases, and could be the potential therapeutic target for cardiovascular diseases. In this review, we summarize the molecular mechanisms regulating ferroptosis, inducers or inhibitors of ferroptosis, and the current progresses of ferroptosis in cardiovascular diseases. Furthermore, we discuss the emerging challenges and future perspectives, which may provide novel insights into the treatment of cardiovascular diseases.

Gastrodin prevents myocardial injury in sleep-deprived mice by suppressing ferroptosis through SIRT6

“…Cardiomyocytes are now considered non-regenerative cells in the body, and it is generally accepted that the more functionally normal cardiomyocytes there are in cardiovascular diseases, the higher the cellular vitality and the better the cardiac function (Yao et al, 2024). Iron-dependent lipid peroxidation accumulation, which causes cellular damage, is one of the pathogenic mechanisms of various cardiac diseases, including myocardial infarction and myocarditis (Zhang and Guo, 2023). Increasing evidence supports that SD precipitates myocardial tissue damage through the induction of ferroptosis (Yuan et al, 2024).…”