ArticleMolecular biotechnology2025
Platelet-Derived Microvesicles Mediate Cardiomyocyte Ferroptosis by Transferring ACSL1 During Acute Myocardial Infarction.
Article in Molecular biotechnology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Integrated bioinformatics analysis, machine learning, and experimental validation reveal that ACSL1 drives myocardial ischemia reperfusion injury via ferroptosis.Journal of bioenergetics and biomembranes · 2026Article
- Integrative transcriptomic analysis and experimental validation identify GPR97 and PROK2 as novel genes upregulated in acute myocardial infarction.Functional & integrative genomics · 2026Article
- Dihydromyricetin confers protection against myocardial ischemia-reperfusion injury by inhibiting ferroptosis through direct targeting of PPARα.Frontiers in pharmacology · 2026Article
- Article
- Exosomes: bridge metabolic regulation in cardiac repair.npj biomedical innovations · 2025Review
- Microvesicle-Shuttled microRNA-130b Activates the Hepatic Inflammation by Inhibiting Glucocorticoid-Receptor-Mediated Immunosuppression in High-Fat Diet-Induced Obese Mice.Veterinary sciences · 2024Article
- Quantitative Proteomic Analysis of Macrophages Infected withInternational journal of molecular sciences · 2024Article
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Authors and funding
7 authors.
Funding
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Abstract
Acute myocardial infarction (AMI) is one of the critical health conditions often caused by the rupture of unstable coronary artery plaque, triggering a series of events, such as platelet activation, thrombus formation, coronary artery blockage, lasted severe ischemia, and hypoxia in cardiomyocytes, and culminating in cell death. Platelet-derived microvesicles (PMVs) act as intermediates for cellular communication. Nevertheless, the role of PMVs in myocardial infarction remains unclear. Initially, AMI-related messenger ribose nucleic acid (mRNA) and micro RNA (miRNA) datasets from the Gene Expression Omnibus (GEO) database were analyzed, specifically focusing on the expressed genes associated with Ferroptosis. Further, a miRNA-mRNA regulatory network specific to AMI was constructed. Then, the effect of PMVs on cardiomyocyte survival was further confirmed through in vitro experiments. High ACSL1 expression was observed in the platelets of AMI patients. The gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses revealed that ACSL1, located in the mitochondria, played a key role in the PPAR signaling pathway. The elevated ACSL1 expression in a co-culture model of PMVs and AC16 cardiomyocytes significantly increased the AC16 cell Ferroptosis. Further, we validated that the platelet ACSL1 expression could be regulated by hsa-miR-449a. Together, these findings suggested that platelet ACSL1 could trigger myocardial cell death via PMV transport. In addition, this research provided a theoretical framework for attenuating myocardial cell Ferroptosis in patients with acute myocardial infarction.
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