LAUSR

Atherosclerosis (AS) is a chronic inflammatory disease of the blood vessels, which is mainly characterized by the form of atherosclerotic plaques and vascular endothelial injury. Its formation involves abnormal lipid metabolism, oxidative stress and inflammation, as well as other processes. AS is the direct cause of various acute cardiovascular and cerebrovascular diseases, such as acute myocardial infarction and acute ischemic stroke. Early intervention in the atherosclerotic inflammatory process and lesion progression is beneficial, and has been associated with the primary prevention of a range of related diseases. Ferroptosis is a non-apoptotic form of cell death different from cell necrosis and autophagy, which has been shown to participate in atherogenesis and atherosclerotic progression through numerous signaling pathways. The main characteristic of ferroptosis is the formation of high levels of cellular iron catalytic free radicals, unsaturated fatty acid accumulation and iron-induced lipid reactive oxygen species accumulation, which can cause oxidative stress, and subsequent DNA, protein and lipid damage. There are numerous hypotheses about the pathogenesis of AS. At present, it has been suggested that ferroptosis can accelerate the progression of AS and that inflammation is associated with the whole process of AS. The mechanisms and signaling pathways related to the involvement of neuroinflammation and ferroptosis in the progression of AS, and therapeutic targets associated with ferroptosis have not yet been elucidated. The present review article evaluated the involvement of ferroptosis in the progression of AS from the perspectives of ferroptotic cell death, the pathogenesis of AS and nervous system inflammation, with the aim of exploring new therapeutic targets for AS.