ArticleNature communications2026
CD177⁺ neutrophil-platelet aggregates contribute to thromboinflammation via NETs in necrotizing enterocolitis.
Article in Nature communications, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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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
5 citing papers in PubMed.
- Platelets mediate fibrin-induced thromboinflammation and NETosis through a GPVI-polyphosphate-FXIIa procoagulant axis.Blood vessels, thrombosis & hemostasis · 2026Article
- RPS29 as a potential early diagnostic biomarker for necrotizing enterocolitis: validation from transcriptomic and proteomic cohorts.Translational pediatrics · 2026Article
- CD177⁺ neutrophil-platelet aggregates contribute to thromboinflammation via NETs in necrotizing enterocolitis.Nature communications · 2026Article
- Neutrophil extracellular traps in asthma and chronic obstructive pulmonary disease: pathogenic roles, and therapeutic opportunities.Frontiers in immunology · 2026Review
- Stage-specific neutrophil states in neonatal injury: from antimicrobial deficiency to pro-resolution repair.Frontiers in immunology · 2026Review
Corrections and comments
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Authors and funding
17 authors.
Funding
Abstract
Necrotizing enterocolitis (NEC) is a severe gastrointestinal disease affecting premature infants, yet its precise pathogenic mechanisms remain unclear. While immunothrombosis, an interplay between inflammation and coagulation, is well recognized in systemic inflammatory diseases, its role in NEC pathogenesis and local intestinal regulation has been incompletely characterized. Here, we combine multi-omics profiling, histopathological analyses, and functional studies using clinical NEC samples and neonatal mouse models. We demonstrate prominent intestinal thromboinflammation in NEC, histologically characterized by immunothrombosis with infiltrating CD177⁺ neutrophils, activated platelets, and fibrin deposition. We show that extensive formation of CD177⁺ neutrophil-platelet aggregates (NPAs) amplifies intestinal injury through neutrophil extracellular trap (NET)-mediated thromboinflammation. Blocking CD177⁺ NPAs or inhibiting NET formation significantly alleviates NEC severity in mouse models. Clinically, elevated CD177⁺ NPA levels correlate with NEC severity and increased thrombotic biomarkers, highlighting their potential as diagnostic and prognostic biomarkers. Importantly, prophylactic administration of low-molecular-weight heparin (LMWH) disrupts NPA formation, reduces NET burden, and improves survival in experimental NEC. Collectively, these findings establish CD177⁺ NPAs as central drivers of NEC pathogenesis, support a thromboinflammatory framework for NEC, and highlight LMWH therapy and CD177⁺ NPA monitoring as possible clinically translatable strategies for neonatal care.
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