ArticleDigestive diseases and sciences2025
Targeting TREM1 Ameliorates Necrotizing Enterocolitis in Neonatal Mice by Inhibiting Endoplasmic Reticulum Stress and Regulating Macrophage Polarization.
Article in Digestive diseases and sciences, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
2 citing papers in PubMed.
- A Potentially TREMendous Treatment: TREM1 Inhibition as a Novel Therapy for Necrotizing Enterocolitis.Digestive diseases and sciences · 2025Article
- TREM-1 inhibitor specificity and timing of treatment initiation can impact its therapeutic efficacy in cancer and inflammatory disease.Frontiers in oncology · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveThis study aims to investigate the role of TREM1 in necrotizing enterocolitis (NEC).
methodsA mouse model of NEC was established through artificial feeding combined with hypoxia-cold stress. Intestinal injury was assessed via H&E staining. Inflammatory cytokines were measured by ELISA, and reactive oxygen species (ROS) activity was evaluated using DHE staining. Intestinal permeability was determined by the fluorescein-isothiocyanate-dextran (FITC-dextran) method. Tight junction proteins were analyzed through immunohistochemistry and western blotting. The expression of CD86 and CD206 in M1 and M2 macrophages was assessed by immunofluorescence, and the mRNA levels of M1 and M2 markers (CD86, iNOS, CD206, and Arg-1) were detected by RT-qPCR. Proteins involved in ER stress were analyzed using western blotting.
resultsInhibition of TREM1 was found to reduce intestinal injury, inflammation, and oxidative stress, improve intestinal barrier function, suppress M1 macrophage polarization, and attenuate ER stress in NEC mice. Moreover, we found that treatment with the ER stress inducer tunicamycin reversed these protective effects of TREM1 inhibition.
conclusionTREM1 inhibition protects against intestinal injury, inflammation, oxidative stress, intestinal barrier damage, and M1 macrophage polarization in NEC mice by suppressing ER stress.
Indexed as
Identifiers
40553398What OpenQuestion holds
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.