ArticleBiomedicines2024
Platelets Induce Cell Apoptosis of Cardiac Cells via FasL after Acute Myocardial Infarction.
Article in Biomedicines, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
2 citing papers in PubMed.
- Elevated IL-1 Beta Plasma Levels, Altered Platelet Activation and Cardiac Remodeling Lead to Moderately Decreased LV Function in Alzheimer Transgenic Mice After Myocardial Ischemia and Reperfusion.Journal of cardiovascular development and disease · 2026Article
- Acute Myocardial Infarction: Molecular Pathogenesis, Diagnosis, and Clinical Management.MedComm · 2025Review
Corrections and comments
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Authors and funding
10 authors.
Funding
Abstract
Acute myocardial infarction (AMI) is one of the leading causes of death worldwide. Cell apoptosis in the myocardium plays an important role in ischemia and reperfusion (I/R) injury, leading to cardiac damage and dysfunction. Platelets are major players in hemostasis and play a crucial role in vessel occlusion, inflammation, and cardiac remodeling after I/R. Here, we studied the impact of platelets on cell apoptosis in the myocardium using a close-chest mouse model of AMI. We found caspase-3-positive resident cardiac cells, while leukocytes were negative for caspase-3. Using two different mouse models of thrombocytopenia, we detected a significant reduction in caspase-3 positive cells in the infarct border zone after I/R injury. Further, we identified platelet FasL to induce cell apoptosis via the extrinsic pathway of Fas receptor activation of target cells. Mechanistically, hypoxia triggers platelet adhesion to FasR, suggesting that platelet-induced apoptosis is elevated after I/R. Platelet-specific FasL knock-out mice showed reduced
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Registered trials
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