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Insight into myocardial ischemia-reperfusion injury from the perspective of ferroptosis
Xia Huang1, Yanni Wang1, Xiangrong Cui2
1Department of Clinical Laboratory of Shanxi Provincial People's Hospital, Shanxi Medical University, Taiyuan, China.
Abstract:
Myocardial ischemia-reperfusion injury (MIRI) most frequently happens in acute myocardial infarction (AMI) when rapid reperfusion is utilized to save the ischemia myocardium. MIRI is the main contributing of poor healing in AMI and is related to high mortality and disability rates around the worldwide. Currently, there is no effective precautionary measure for MIRI. Ferroptosis is a novel regulated cell death characterized by iron overload and reactive oxygen species (ROS) accumulation, which lead to death membrane lipid peroxidation. An increasing amount of studies indicates that ferroptosis plays a vital role in the occurrence and progression of MIRI. Given the crucial role of ferroptosis in MIRI, it is critical to understand the cardiomyocyte iron metabolism and investigate the molecular mechanisms of ferroptosis. In this review, we systematically summarize the molecular and metabolic pathways of ferroptosis in context of MIRI, which could provide novel understandings for the pathophysiological machine and new ideas for treatment.
Insights
Myocardial ischemia-reperfusion injury (MIRI) is a major complication of acute myocardial infarction (AMI). This review explores how ferroptosis, a cell death pathway involving iron, contributes to MIRI, offering insights for new treatments.
Area of Science:
- Cardiology
- Cell Biology
- Pathophysiology
Background:
- Myocardial ischemia-reperfusion injury (MIRI) is a significant complication following acute myocardial infarction (AMI) treatment.
- MIRI contributes to poor cardiac healing, high mortality, and disability rates globally.
- Currently, effective preventative strategies for MIRI are lacking.
Purpose of the Study:
- To systematically review the molecular and metabolic pathways of ferroptosis in the context of MIRI.
- To elucidate the role of cardiomyocyte iron metabolism and ferroptosis mechanisms in MIRI.
- To provide novel insights into the pathophysiology of MIRI and identify potential therapeutic targets.
Main Methods:
- Literature review focusing on ferroptosis and MIRI.
- Analysis of molecular and metabolic pathways involved in ferroptosis.
- Examination of the role of iron metabolism in cardiomyocytes during MIRI.
Main Results:
- Ferroptosis, characterized by iron overload and reactive oxygen species (ROS) accumulation, is increasingly recognized as a key player in MIRI.
- Lipid peroxidation of cell membranes is a hallmark of ferroptosis-induced cell death in MIRI.
- Understanding ferroptosis pathways is critical for developing MIRI treatments.
Conclusions:
- Ferroptosis plays a vital role in the occurrence and progression of MIRI.
- Investigating cardiomyocyte iron metabolism and ferroptosis mechanisms is crucial for MIRI research.
- This review provides a foundation for developing novel therapeutic strategies against MIRI.
