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Platelet Internalization Mediates Ferroptosis in Myocardial Infarction
Shuo Miao1, Qingsong Zhang2, Wei Ding2
1School of Basic Medicine, Qingdao University, China (S.M., M.L., L.Y., J.Z., J.W.).
Arteriosclerosis, Thrombosis, and Vascular Biology
|November 10, 2022
Summary
Platelets contribute to heart attack injury by releasing miR-223-3p, which causes cardiomyocyte death via ferroptosis. Targeting this pathway may offer new treatments for myocardial infarction.
Area of Science:
- Cardiovascular Biology
- Molecular Medicine
- Hematology
Background:
- Myocardial infarction (heart attack) involves cardiomyocyte death and inflammation, with platelets playing a known role in injury.
- The direct role of platelets in regulating cardiomyocyte death during myocardial infarction remains unclear.
Purpose of the Study:
- To elucidate the mechanism by which platelets contribute to cardiomyocyte death in myocardial infarction.
- To investigate the direct regulation of cardiomyocyte death by platelets.
Main Methods:
- Utilized a myocardial infarction mouse model and human patient specimens.
- Investigated platelet internalization and its molecular consequences within cardiomyocytes.
Main Results:
- Myocardial infarction leads to platelet internalization and release of platelet-enriched microRNA-223-3p (miR-223-3p).
- miR-223-3p targets ACSL3 in cardiomyocytes, reducing stearic acid-phosphatidylcholine, a protective molecule against ferroptosis.
- This process results in ferroptosis-induced cardiomyocyte death.
Conclusions:
- Revealed a novel mechanism of platelet-mediated myocardial injury through ferroptosis.
- Suggests antiplatelet therapies could offer multi-mechanism benefits for myocardial infarction.
- Highlights ferroptosis as a potential therapeutic target for myocardial infarction treatment.
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