Evidence map›Paper›PMID 41722854›Full record

ArticleCellular and molecular gastroenterology and hepatology2026

Glial Connexin-43 Is a Pathogenic Mechanism Promoting Gut Inflammation in Postoperative Ileus Induced by Gut Surgical Manipulation With Potential Relevance to Humans.

Samhita Chaudhuri, Reiner Schneider, Dmitrii Pavlov, Alix Zuleta Alarcon, Elvio Mazzotta, Jonathon L McClain, Patrick Leven, Paolo Fadda, Manekeller Steffen, Yunpeng Du and 4 more

Abstract read
In one paragraph

Article in Cellular and molecular gastroenterology and hepatology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

1 citing paper in PubMed.

  1. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

14 authors.

Samhita ChaudhuriDepartment of Anesthesiology, Wexner Medical Center, The Ohio State University, Columbus, Ohio.
Reiner SchneiderDepartment of Surgery, University Clinics of Bonn, Bonn, Germany.
Dmitrii PavlovDepartment of Anesthesiology, Wexner Medical Center, The Ohio State University, Columbus, Ohio.
Alix Zuleta AlarconDepartment of Anesthesiology, Wexner Medical Center, The Ohio State University, Columbus, Ohio.
Elvio MazzottaDepartment of Anesthesiology, Wexner Medical Center, The Ohio State University, Columbus, Ohio.
Jonathon L McClainDepartment of Physiology, Michigan State University, East Lansing, Michigan.
Patrick LevenDepartment of Surgery, University Clinics of Bonn, Bonn, Germany.
Paolo FaddaComprehensive Cancer Center, Genomics Shared Resource, The Ohio State University, Columbus, Ohio.
Manekeller SteffenDepartment of Surgery, University Clinics of Bonn, Bonn, Germany.
Yunpeng DuDepartment of Anesthesiology, Wexner Medical Center, The Ohio State University, Columbus, Ohio.
Alan HarzmanDepartment of Anesthesiology, Wexner Medical Center, The Ohio State University, Columbus, Ohio.
Brian D GulbransenDepartment of Physiology, Michigan State University, East Lansing, Michigan.
Sven WehnerDepartment of Surgery, University Clinics of Bonn, Bonn, Germany.
Fievos L ChristofiDepartment of Anesthesiology, Wexner Medical Center, The Ohio State University, Columbus, Ohio. Electronic address: fedias.christofi@osumc.edu.

Funding

Enteric glial ETBR signaling in postoperative ileusR01DK125809 · NIDDK · OHIO STATE UNIVERSITY · PI CHRISTOFI, FEDIAS LEONTIOU · 2020 to 2023
$1.6M
Enteric Glial Mechanotransduction and Mechanical Stress Induced Postoperative IleusR01DK141842 · NIDDK · OHIO STATE UNIVERSITY · PI FEDIAS LEONTIOU CHRISTOFI · 2025 to 2026
$1.0M
NIDDK NIH HHS R01 DK125809NIDDK NIH HHS R01 DK141842
6 · The paper itself

Abstract

BACKGROUND &

aimsAbdominal surgery often precipitates postoperative ileus (POI), a frequent and severe gastrointestinal (GI) motility disorder, through mechanisms that involve intestinal inflammation. Emerging data show that enteric glia acquire a reactive phenotype that aggravates POI, but how glia exert this effect remains unclear. Enteric glia express connexin-43 hemichannels (gCx43), which are implicated in neurological and inflammatory disorders. Thus, we aimed to decipher contributions of glial connexin-43 (Cx43) in the pathophysiology of POI.

methodsWe induced POI in mice using in vivo intestinal manipulation and used glial Cx43cKO (Sox10

resultsCx43 is the highest expressed connexin in enteric glia in mice and humans. Up-regulation of Cx43 occurs in various disease models linked to POI, GI surgical trauma, inflammation, immune cell activation, and enteric gliosis. In the mouse POI model, glial Cx43-deletion reduces glial reactivity, pro-inflammatory signals, upregulates host protection genes, regulates immune cell activation, and prevents enteric neuropathy. In hEGCs, interleukin (IL)-1β induction opens Cx43 and stimulates release of IL-6 and C-C motif ligand 2 (CCL2). The Cx43 peptide inhibitor, 43Gap26, inhibits glial Cx43 activation, reduces IL-6 release, and blocks upregulation of macrophage activation factors and immune cell regulation factors. Surgical intestinal trauma in patients upregulates Cx43 during inflammation and enteric gliosis in mouse POI.

conclusionsGlial Cx43 signaling promotes enteric gliosis, immune cell activation, inflammation, and enteric neuropathy in mice with potential translatability to humans after intestinal surgical trauma and mechanical stress in POI. Interventions that block glial Cx43 activation may be protective against POI development.

Indexed as

Connexin 43IleusInflammationNeurogliaPostoperative ComplicationsAnimalsDisease Models, AnimalEnteric Nervous SystemHumansMaleMiceConnexin 43Cx43 Gap JunctionsCx43 HemichannelsHuman In Vitro StudiesIntestinal InflammationMechanical StressPostoperative IleusReactive Enteric GliaSurgical Trauma

Identifiers

PMID41722854
PMCPMC13123614

What OpenQuestion holds

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LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

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.