ArticleInflammation2026
NMI Promotes Pro-Inflammatory Macrophage Polarization and Exacerbates.
Article in Inflammation, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 1 paper.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed.
- N-myc and STAT interactor promotes poly(I:C)-induced pulmonary coagulopathy via STAT3-dependent tissue factor.Frontiers in immunology · 2026Article
Corrections and comments
- Erratum issued
Authors and funding
16 authors.
Funding
Abstract
Macrophages polarization is critical in the pathogenesis of ulcerative colitis (UC). However, the endogenous regulators of this process remain poorly understood. Here, we investigate the role of the damage-associated molecular pattern (DAMP), N-myc and STAT interactor (NMI), in driving pro-inflammatory (M1) macrophages polarization and UC progression. Analysis of three of independent inflammatory bowel disease (IBD) transcriptomic datasets revealed a significant upregulation of NMI expression in UC patients, with prominent enrichment in macrophages and epithelial cells, a finding recapitulated in dextran sulfate sodium (DSS)-induce murine colitis model. Mice with Nmi gene knock-out (Nmi−/−) were protected from both acute and chronic colitis, exhibiting reduced intestinal M1 macrophages infiltration and low pro-inflammatory cytokine levels. Mechanistically, in vitro studies demonstrate that recombinant NMI promoted M1 macrophages polarization via TLR4-dependent MAPK/AP1 signaling pathway. Therapeutically, administration of an NMI-neutralizing antibody significantly ameliorated colitis by reprogramming the macrophage balance, reducing pro-inflammatory M1 accumulation while increasing anti-inflammatory M2 subsets. Collectively, our study establishes NMI as a key regulator of pro-inflammatory macrophage polarization and highlights its potential as a novel therapeutic target for UC.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.