ArticleCardiovascular therapeutics2026
Role of Circulating Microparticles in Impairing Endothelial Function and Activating Oxidative Stress Is Related to No-Reflow in STEMI.
Article in Cardiovascular therapeutics, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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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
1 citing paper in PubMed.
- Role of Circulating Microparticles in Impairing Endothelial Function and Activating Oxidative Stress Is Related to No-Reflow in STEMI.Cardiovascular therapeutics · 2026Article
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Authors and funding
7 authors.
Funding
Abstract
objectivePatients with ST-segment elevation myocardial infarction (STEMI) frequently experience no-reflow (NRF) during percutaneous coronary intervention (PCI). Nevertheless, the pathogenesis of NRF involves multiple factors and has not been fully elucidated to date. Given that endothelial dysfunction, inflammation, and oxidative stress are jointly implicated in both MP-related processes and NRF occurrence, this study was performed to explore the potential role of circulating microparticles (MPs) in the development of NRF.
methodsMPs were isolated from healthy subjects (n = 30), patients with angina and negative coronary angiography (control, n = 30), and STEMI patients with (n = 30) or without NRF (n = 30). The effects of MPs on endothelium-dependent vasodilatation, the expression of caveolin-1 and endothelial nitric oxide synthase (eNOS), and the production of nitric oxide (NO), superoxide anion (O
resultsCompared with controls and healthy subjects, circulating MP levels were significantly higher in STEMI patients and were further elevated in STEMI patients with NRF. MPs isolated from NRF patients impaired endothelial-dependent vasodilatation, decreased the expression of phosphorylated eNOS at Ser1177, reduced NO production, HCAECs proliferation, and endothelial tube formation, but upregulated the expression of caveolin-1 and phosphorylated eNOS at Thr495, and increased the generation of O
conclusionsCirculating MPs are associated with NRF in the clinical context and induce endothelial dysfunction in experimental models. Our findings provide new insight into the underlying molecular mechanisms of NRF in STEMI in experimental models.
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