ArticleBasic research in cardiology2025
Molecular screening in a translational large animal trial identifies a differential inflammatory response for MINOCA.
Article in Basic research in cardiology, 2025. 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.
- Molecular mechanisms of coronary microembolization-induced MINOCA.Basic research in cardiology · 2026Review
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Authors and funding
21 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Myocardial infarction without obstructive coronary arteries (MINOCA) comprises up to 15% of all myocardial infarctions (MI) and could be caused by cardiac microembolization (CME) originating from plaque rupture and/or erosion. Early diagnosis remains a challenge due to limited early biomarkers, leading to high morbidity. Here, we have systematically characterized acute (up to 5 h) CME-induced MINOCA in comparison to MI using clinical markers, histology, multi-ELISAs, miRNA profiling, and proteomics in a translational porcine animal model. CME-induced MINOCA model was created by injecting autologous microthrombi, generated by carotid crush maneuver, into the coronary arteries, whereas MI was induced by LAD balloon occlusion/reperfusion. MINOCA animals exhibited low troponin (547.0 ± 489.2 ng/L) and creatine kinase (1827.8 ± 677.3 U/L) levels, as well as infarct size (2.3 ± 0.8%), necrosis (7.6 ± 3.2%), and interstitial hemorrhage (0.6 ± 0.4%). Immune cell infiltration surrounding MINOCA microthrombi sites was significantly higher (1532 ± 722 cells/mm
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