ANNALS OF CLINICAL AND ANALYTICAL MEDICINE, cilt.17, sa.1, ss.87-94, 2026 (ESCI)
This review comprehensively explores the interplay between ferroptosis, pyroptosis, and the pathogenesis of atherosclerosis, a chronic vascular inflammatory disorder. It offers an in-depth analysis of atherosclerosis, emphasizing its status as a prevalent and fatal group of cardiovascular diseases. The etiology of cardiovascular diseases is discussed, with a particular emphasis on atherosclerosis as a chronic process characterized by the accumulation of lipid and fibrous elements in the arteries. The pathogenesis of atherosclerosis, from the formation of plaque/atheroma to the progression of atherosclerotic lesions, is detailed, shedding light on the critical role of foam cells, endothelial dysfunction, and inflammatory mediators in this process. Furthermore, the article thoroughly examines the relatively recent concepts of ferroptosis and pyroptosis and their implications in atherosclerosis. Ferroptosis, described as a form of programmed cell death characterized by iron accumulation and reactive oxygen species, is scrutinized in the context of atherosclerosis. The molecular mechanisms underlying ferroptosis, including oxidative membrane damage and iron metabolism, are elucidated. Similarly, pyroptosis, a regulated cell death process involving the release of proinflammatory cytokines and pore formation in the cytoplasmic membrane, is meticulously discussed in atherosclerosis. The involvement of vascular endothelial cells, vascular smooth muscle cells, and macrophages in the pathophysiology of ferroptosis and pyroptosis during atherosclerosis is also thoroughly explored. Overall, the article offers valuable insights into the potential therapeutic targets presented by ferroptosis and pyroptosis in the treatment of atherosclerosis, paving the way for further research and clinical implications in this field.