ArticleScience advances2025
Platelets induce endothelial cell mitochondrial dysfunction in myocardial infarction.
Article in Science advances, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Divergent Effects of GnRH Agonist and GnRH Antagonist Treatment on Platelet Activity and Transcriptome.JACC. CardioOncology · 2026Article
- Cardiac-targeted delivery of miRNA via antioxidant nanozymes ameliorates cardiac dysfunction and fibrosis after myocardial infarction.Journal of nanobiotechnology · 2026Article
- Multi-omics analyses reveal novel metabolic signatures of post-traumatic deep vein thrombosis in patients with coronary heart disease.Metabolomics : Official journal of the Metabolomic Society · 2026Article
- Endothelial PTBP1 Deletion in Transplanted Cardiac Tissue Limits Cardiac Allograft Vasculopathy.bioRxiv : the preprint server for biology · 2026Article
Corrections and comments
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Authors and funding
11 authors.
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Abstract
Coronary endothelial dysfunction plays a key role in the pathogenesis of acute coronary syndromes. During myocardial infarction (MI), activated platelets release prothrombotic and proinflammatory factors, contributing to vascular injury and dysfunction. To investigate platelet-mediated endothelial dysfunction, endothelial cells (ECs) were treated with platelet-released factors from patients with MI and non-MI controls undergoing coronary angiography. RNA sequencing revealed that MI platelets induced EC mitochondrial dysfunction, confirmed by reduced mitochondrial membrane potential and disrupted mitochondrial networks. Integrating platelet transcriptomic data, we identified the C-C motif chemokine ligand 3 (CCL3) as significantly up-regulated in MI platelets and a key mediator of EC mitochondrial dysfunction. Blocking its receptor, CCR5, attenuated CCL3 effects. In an independent cohort of 261 patients with established cardiovascular disease, higher circulating CCL3 levels were associated with incident major adverse cardiovascular events. Together, these findings establish a mechanistic link between platelet activation and coronary endothelial dysfunction in MI.
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Registered trials
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