ArticlePloS one2025
Extraction of coronary thrombus-derived exosomes from patients with acute myocardial infarction and its effect on the function of adventitial cells.
Article in PloS one, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- High levels of cell-free hemoglobin and iron in cerebral thrombi of pre-Omicron COVID-19 stroke patients: novel drivers of SARS-CoV-2-induced prothrombotic state.Acta neuropathologica · 2026Article
- Exosomal lncRNA FENDRR Orchestrates Immune Remodelling and Ferroptosis in the Comorbidity of Lung Cancer and Type 1 Myocardial Infarction.Human mutation · 2026Article
- Plasma small-extracellular vesicles' proteomic signature in neoadjuvant chemotherapy-naïve breast cancer patients.PloS one · 2026Article
- Multi-omics approach to personalised treatment: insights into thrombus-derived exosome regulation in cardiomyocyte ferritinophagy.Frontiers in immunology · 2025Article
- Role of thrombus-derived exosomal lncRNA LOC101928697 in regulating endothelial function via FUS protein interaction in myocardial infarction.Science progressArticle
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Authors and funding
5 authors.
Funding
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Abstract
backgroundType I acute myocardial infarction (T1MI) has a very high morbidity and mortality rate. The role of thrombus-derived exosomes (TEs) in T1MI is unclear.
methodsThe objective of this study was to identify the optimal thrombolytic drug and concentration for extracting TEs. To this end, a series of time and concentration combinations were tested. Subsequently, the effect of TEs on thrombus-adjacent cells was investigated. Finally, we conducted lncRNA microarray analysis on the extracted TEs (GSE213115).
resultsTEs has been demonstrated to promote necrosis, autophagy, and ferroptosis of human cardiomyocytes, while inhibiting the proliferation and migration of human umbilical vein endothelial cells (HUVECs). Furthermore, TEs can stimulate the proliferation and migration of smooth muscle cells, and induce a transformation from a contractile to a secretory phenotype. Bioinformatics analysis revealed that five lncRNAs, AC068418.2, AC010186.3, AL031430.1, AC121333.1, and AL136526.1, exhibited significant differential expression in TE and regulated cell autophagy and ferroptosis by directly binding to TP53, TP63, and RELA, respectively.
conclusionsWe demonstrate that TEs as a potential target and research direction for the treatment of heart failure after T1MI. TEs may regulate ferroptosis and autophagy in thrombus-adjacent cells through the enrichment of certain lncRNAs.
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