Research status and prospective directions of ferroptosis in the pathogenesis of vascular calcification.

Ferroptosis is a recently identified form of regulated cell death, characterized by iron-dependent accumulation of intracellular reactive oxygen species. It plays a significant role in the onset and progression of various immune-mediated diseases and has become a focal point in contemporary biomedical research. Vascular calcification (VC) is associated with a range of cardiovascular diseases, including myocardial infarction stroke, aortic and peripheral artery disease, heart failure, chronic kidney disease, diabetes mellitus, and aortic valve stenosis, posing significant threats to public health. However, therapeutic options remain limited, highlighting the urgent need for further investigation. In recent years, several pioneering studies have indicated that ferroptosis activation significantly contributes to the progression of VC. These findings have attracted growing attention from researchers across related disciplines. Nevertheless, the underlying mechanisms are not yet fully understood, indicating the necessity for further exploration. This study focuses on a special review of the molecular regulatory pathways of ferroptosis and VC, systematically summarizes the confirmed core pathways, explores the potential regulatory directions, and discusses the clinical transformation value combined with the mechanism, so as to provide exclusive and practical theoretical reference and research ideas for the in-depth research in this field and the targeted therapy of VC.