The Chains of Ferroptosis Interact in the Whole Progression of Atherosclerosis

Atherosclerosis (AS), a category of cardiovascular disease (CVD) that can cause other more severe disabilities, increasingly jeopardizes human health. Owing to its imperceptible and chronic symptoms, it is hard to determine the pathogenesis and precise therapeutics for AS. A novel type of programmed...

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Published inJournal of inflammation research Vol. 16; pp. 4575 - 4592
Main Authors Wan, Xueqi, Zhang, Huan, Tian, Jinfan, Hao, Peng, Liu, Libo, Zhou, Yuquan, Zhang, Jing, Song, Xiantao, Ge, Changjiang
Format Journal Article
LanguageEnglish
Published Dove Medical Press Limited 31.10.2023
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Summary:Atherosclerosis (AS), a category of cardiovascular disease (CVD) that can cause other more severe disabilities, increasingly jeopardizes human health. Owing to its imperceptible and chronic symptoms, it is hard to determine the pathogenesis and precise therapeutics for AS. A novel type of programmed cell death called ferroptosis was discovered in recent years that is distinctively different from other traditional cell death pathways in morphological and biochemical aspects. Characterized by iron overload, redox disequilibrium, and accumulation of lipid hydroperoxides (L-OOH), ferroptosis influences endothelial cells, vascular smooth muscle cells (VSMCs), and macrophages, as well as inflammation, partaking in the pathology of many cardiovascular diseases such as atherosclerosis, stroke, ischemia-reperfusion injury, and heart failure. The mechanisms behind ferroptosis are so sophisticated and interwoven that many molecules involved in this procedure are unknown. This review systematically depicts the initiation and modulation of ferroptosis and summarizes the contribution of ferroptosis to AS, which may open a feasible approach for target treatment in the alleviation of AS progression. Keywords: ferroptosis, iron overload, oxidation, lipid peroxidation, atherosclerosis
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These authors contributed equally to this work
ISSN:1178-7031
1178-7031
DOI:10.2147/JIR.S430885