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Author Spotlight: Tracing the Ferroptotic Signatures and Cell Death Dynamics in Medulloblastoma for Advanced Therapeutics
Published on: March 15, 2024
Ferroptosis: a potential target for the treatment of atherosclerosis
Chengyi Li1, Ran Liu1, Zhenyu Xiong1
1School of Medicine, Yangtze University, Jingzhou 434020, China.
Insights
Ferroptosis, an iron-dependent cell death, drives atherosclerosis progression by increasing oxidative stress and lipid peroxidation. Targeting ferroptosis offers a novel therapeutic strategy for cardiovascular events like heart attack and stroke.
Area of Science:
- Biomedical Science
- Cardiovascular Research
- Cell Death Mechanisms
Background:
- Atherosclerosis (AS) is a primary cause of heart attack and stroke, marked by plaque instability and cell death.
- Ferroptosis, a newly identified iron-dependent cell death, plays a significant role in AS progression.
- Elevated intracellular iron in AS exacerbates oxidative stress, lipid peroxidation, and inflammation, impacting vascular cell function.
Approach:
- This review systematically examines the intricate relationship between ferroptosis and atherosclerosis.
- It elucidates the molecular mechanisms linking ferroptosis to AS development and progression.
- The review proposes ferroptosis inhibition as a potential therapeutic avenue for AS.
Key Points:
- Ferroptosis contributes to AS by increasing reactive oxygen species (ROS) and lipid peroxidation.
- Accumulated iron activates pathways implicated in AS, including abnormal lipid metabolism and inflammation.
- Ferroptosis dysregulates the function of macrophages, vascular smooth muscle cells, and endothelial cells.
Conclusions:
- Understanding the molecular interplay between ferroptosis and AS is crucial.
- Targeting ferroptosis presents a promising strategy to inhibit AS progression and prevent cardiovascular events.
- Further research into ferroptosis pathways could unlock novel treatments for atherosclerosis.
Abstract:
Atherosclerosis (AS), the main contributor to acute cardiovascular events, such as myocardial infarction and ischemic stroke, is characterized by necrotic core formation and plaque instability induced by cell death. The mechanisms of cell death in AS have recently been identified and elucidated. Ferroptosis, a novel iron-dependent form of cell death, has been proven to participate in atherosclerotic progression by increasing endothelial reactive oxygen species (ROS) levels and lipid peroxidation. Furthermore, accumulated intracellular iron activates various signaling pathways or risk factors for AS, such as abnormal lipid metabolism, oxidative stress, and inflammation, which can eventually lead to the disordered function of macrophages, vascular smooth muscle cells, and vascular endothelial cells. However, the molecular pathways through which ferroptosis affects AS development and progression are not entirely understood. This review systematically summarizes the interactions between AS and ferroptosis and provides a feasible approach for inhibiting AS progression from the perspective of ferroptosis.
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