ArticleFrontiers in pediatrics2025
Platelet specific knockout of integrin beta-3 (β3) reduces severity of necrotizing enterocolitis in murine neonates.
Article in Frontiers in pediatrics, 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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1 citing paper in PubMed.
- The role of myeloid cells in the pathogenesis of necrotizing enterocolitis; a scoping review.Frontiers in pediatrics · 2026Review
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10 authors.
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Abstract
Introduction: Necrotizing Enterocolitis (NEC) is the most impactful gastrointestinal disease of premature neonates and preclinical evidence shows that the event of platelet activation is an important pathophysiological contributor during NEC-like injury in murine neonates. Integrin αIIb/β3 (glycoprotein [GP]IIb/IIIa) is the primary platelet activation marker showing increased platelet-monocytes aggregation during NEC-like injury. The present study investigates whether platelet lineage-specific deletion of integrin-β3 reduces NEC-like injury in murine neonates. Methods: C57BL/6 and integrin-β3 Results: Integrin-β3-associated platelet-monocyte aggregation was significantly observed in the intestine and blood of murine NEC-like injury and in the human NEC intestine. Platelet-specific deletion of integrin-β3's exon-1 leads to inhibition of platelet-monocyte aggregation in circulating blood and intestine, thus reducing the resulting intestinal injury and the level of inflammatory activation cytokines in the blood. Conclusion: Monocyte-platelet aggregation is an important pathophysiological event and the blockade of integrin-β3 merits a potential therapeutic target in NEC.
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