Purpose of Review
This review aims to elucidate the multifaceted role of iron in the pathogenesis of atherosclerosis. The primary objective is to summarize recent advances in understanding how iron contributes to atherosclerosis through various cellular mechanisms. Additionally, the review explores the therapeutic implications of targeting iron metabolism in the prevention and treatment of cardiovascular diseases.
Recent Findings
A growing body of literature suggests that excess iron accelerates the progression of atherosclerosis, with the deleterious form of iron, non-transferrin-bound iron (NTBI), particularly exacerbating this process. Furthermore, iron overload has been demonstrated to play a pivotal role in endothelial cells, vascular smooth muscle cells, and macrophages, contributing to plaque instability and disease progression by promoting lipid peroxidation, oxidative stress, inflammatory responses, and ferroptosis.
Summary
Iron plays a complex role in atherosclerosis, influencing multiple cellular processes and promoting disease progression. By promoting oxidative stress, inflammation, and ferroptosis, iron exacerbates endothelial dysfunction, smooth muscle cell calcification, and the formation of macrophage-derived foam cells. Targeted therapies focusing on iron metabolism have proven effective in treating atherosclerosis and other cardiovascular diseases.
