Ferroptosis: A Key Driver in Atherosclerosis Progression and Arterial Disease

Atherosclerosis (AS) is a growing global health epidemic and is the leading cause of cardiovascular health problems, including ischemic stroke, coronary artery disease, and peripheral vascular disease. Despite extensive research on the underlying mechanisms of AS, iron remains an under-investigated...

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Main Authors: Amr Elkammash, Abrar Zaki, Omar Tawfik, Sherif Gouda
Format: Article
Language:English
Published: IMR Press 2024-12-01
Series:Reviews in Cardiovascular Medicine
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Online Access:https://www.imrpress.com/journal/RCM/25/12/10.31083/j.rcm2512441
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author Amr Elkammash
Abrar Zaki
Omar Tawfik
Sherif Gouda
author_facet Amr Elkammash
Abrar Zaki
Omar Tawfik
Sherif Gouda
author_sort Amr Elkammash
collection DOAJ
description Atherosclerosis (AS) is a growing global health epidemic and is the leading cause of cardiovascular health problems, including ischemic stroke, coronary artery disease, and peripheral vascular disease. Despite extensive research on the underlying mechanisms of AS, iron remains an under-investigated mediator in the atherosclerotic process. Iron’s involvement in AS is primarily linked to the iron-induced programmed cell death process known as ferroptosis. Ferroptosis is initiated in endothelial cells when iron overload triggers the Fenton reaction, resulting in the production of reactive oxygen species (ROS) and lipid peroxides. This oxidative stress damages cellular components, ultimately leading to cell death. The review examines the role of iron overload and ferroptosis in the progression and instability of atherosclerotic plaques. Additionally, we explore the potential therapeutic roles of iron chelators and ROS scavengers in mitigating the adverse effects of ferroptosis. The findings indicate that ferroptosis contributes significantly to the progression and instability of atherosclerotic plaques by promoting oxidative damage and cellular dysfunction. Iron chelators and ROS scavengers have shown promise in reducing ferroptosis-induced damage in endothelial cells. These therapeutic agents can potentially stabilize atherosclerotic plaques and prevent the progression of AS. Ferroptosis is a critical yet under-explored pathway in the development and progression of atherosclerosis. Targeting iron-induced oxidative stress through iron chelation and ROS scavenging presents a promising therapeutic strategy for mitigating the adverse effects of ferroptosis on atherosclerotic plaque stability. Further research is needed to validate these therapeutic approaches and better understand the molecular mechanisms underlying ferroptosis in atherosclerosis.
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spelling doaj-art-0e2d8c1f8ff745088c0e63585ce1b1a22024-12-30T09:51:26ZengIMR PressReviews in Cardiovascular Medicine1530-65502024-12-01251244110.31083/j.rcm2512441S1530-6550(24)01606-5Ferroptosis: A Key Driver in Atherosclerosis Progression and Arterial DiseaseAmr Elkammash0Abrar Zaki1Omar Tawfik2Sherif Gouda3Department of Cardiology, Bristol Heart Institute, BS2 8HW Bristol, UKDepartment of General Medicine, Eastbourne District General Hospital, BN21 2UD East Sussex, UKDepartment of Cardiology, Bristol Heart Institute, BS2 8HW Bristol, UKDepartment of Cardiology, Royal Gwent Hospital, NP20 2UB Newport, UKAtherosclerosis (AS) is a growing global health epidemic and is the leading cause of cardiovascular health problems, including ischemic stroke, coronary artery disease, and peripheral vascular disease. Despite extensive research on the underlying mechanisms of AS, iron remains an under-investigated mediator in the atherosclerotic process. Iron’s involvement in AS is primarily linked to the iron-induced programmed cell death process known as ferroptosis. Ferroptosis is initiated in endothelial cells when iron overload triggers the Fenton reaction, resulting in the production of reactive oxygen species (ROS) and lipid peroxides. This oxidative stress damages cellular components, ultimately leading to cell death. The review examines the role of iron overload and ferroptosis in the progression and instability of atherosclerotic plaques. Additionally, we explore the potential therapeutic roles of iron chelators and ROS scavengers in mitigating the adverse effects of ferroptosis. The findings indicate that ferroptosis contributes significantly to the progression and instability of atherosclerotic plaques by promoting oxidative damage and cellular dysfunction. Iron chelators and ROS scavengers have shown promise in reducing ferroptosis-induced damage in endothelial cells. These therapeutic agents can potentially stabilize atherosclerotic plaques and prevent the progression of AS. Ferroptosis is a critical yet under-explored pathway in the development and progression of atherosclerosis. Targeting iron-induced oxidative stress through iron chelation and ROS scavenging presents a promising therapeutic strategy for mitigating the adverse effects of ferroptosis on atherosclerotic plaque stability. Further research is needed to validate these therapeutic approaches and better understand the molecular mechanisms underlying ferroptosis in atherosclerosis.https://www.imrpress.com/journal/RCM/25/12/10.31083/j.rcm2512441ferroptosisiron overloadchelationreactive oxygen speciesfenton reactionatherosclerosis
spellingShingle Amr Elkammash
Abrar Zaki
Omar Tawfik
Sherif Gouda
Ferroptosis: A Key Driver in Atherosclerosis Progression and Arterial Disease
Reviews in Cardiovascular Medicine
ferroptosis
iron overload
chelation
reactive oxygen species
fenton reaction
atherosclerosis
title Ferroptosis: A Key Driver in Atherosclerosis Progression and Arterial Disease
title_full Ferroptosis: A Key Driver in Atherosclerosis Progression and Arterial Disease
title_fullStr Ferroptosis: A Key Driver in Atherosclerosis Progression and Arterial Disease
title_full_unstemmed Ferroptosis: A Key Driver in Atherosclerosis Progression and Arterial Disease
title_short Ferroptosis: A Key Driver in Atherosclerosis Progression and Arterial Disease
title_sort ferroptosis a key driver in atherosclerosis progression and arterial disease
topic ferroptosis
iron overload
chelation
reactive oxygen species
fenton reaction
atherosclerosis
url https://www.imrpress.com/journal/RCM/25/12/10.31083/j.rcm2512441
work_keys_str_mv AT amrelkammash ferroptosisakeydriverinatherosclerosisprogressionandarterialdisease
AT abrarzaki ferroptosisakeydriverinatherosclerosisprogressionandarterialdisease
AT omartawfik ferroptosisakeydriverinatherosclerosisprogressionandarterialdisease
AT sherifgouda ferroptosisakeydriverinatherosclerosisprogressionandarterialdisease