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Published on: March 15, 2024
From Iron Metabolism to Ferroptosis: Pathologic Changes in Coronary Heart Disease
Xinbiao Fan1,2, Aolin Li1, Zhipeng Yan1
1First Teaching Hospital of Tianjin University of Traditional Chinese Medicine, Tianjin 300183, China.
Insights
Disordered iron metabolism contributes to coronary heart disease (CHD) through ferroptosis, a cell death pathway. Targeting ferroptosis offers a potential new treatment strategy for CHD.
Area of Science:
- Cardiovascular Science
- Cell Biology
- Biochemistry
Background:
- Coronary heart disease (CHD), a prevalent cardiovascular disease (CVD), is linked to oxidative stress and inflammation.
- Iron, essential for bodily functions, can induce reactive oxygen species (ROS) and lipid peroxidation due to its redox activity.
- Evidence suggests that disrupted iron metabolism, leading to iron overload and ferroptosis, plays a role in CHD pathogenesis.
Purpose of the Study:
- To review iron metabolism mechanisms in cardiomyocytes (CMs).
- To elucidate the connection between iron metabolism and ferroptosis in CHD.
- To highlight the roles of iron metabolism and ferroptosis in CHD progression.
Main Methods:
- Literature review on iron metabolism in cardiomyocytes.
- Analysis of the relationship between iron metabolism and ferroptosis.
- Examination of ferroptosis's role in the pathological progression of CHD.
Main Results:
- Disordered iron metabolism is implicated in the pathological progression of CHD.
- Iron overload can induce ferroptosis, characterized by iron-dependent lipid peroxidation.
- Ferroptosis is suggested to be a key factor in CHD development.
Conclusions:
- Targeting ferroptosis presents a promising therapeutic avenue for CHD.
- Understanding iron metabolism in CMs is crucial for CHD research.
- Ferroptosis mechanisms are integral to the development of CHD.
Abstract:
Coronary heart disease (CHD) is closely related to oxidative stress and inflammatory response and is the most common cardiovascular disease (CVD). Iron is an essential mineral that participates in many physiological and biochemical reactions in the human body. Meanwhile, on the negative side, iron has an active redox capacity, which leads to the accumulation of reactive oxygen species (ROS) and lipid peroxidation. There is growing evidence that disordered iron metabolism is involved in CHD's pathological progression. And the result of disordered iron metabolism is associated with iron overload-induced programmed cell death, often called ferroptosis. That features iron-dependent lipid peroxidation. Ferroptosis may play a crucial role in the development of CHD, and targeting ferroptosis may be a promising option for treating CHD. Here, we review the mechanisms of iron metabolism in cardiomyocytes (CMs) and explain the correlation between iron metabolism and ferroptosis. Meanwhile, we highlight the specific roles of iron metabolism and ferroptosis in the main pathological progression of CHD.
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