Evidence map›Paper›PMID 38280053›Full record

ReviewInflammatory bowel diseases2024

Breaking Down Barriers: Epithelial Contributors to Monogenic IBD Pathogenesis.

Jodie D Ouahed, Alexandra Griffith, Lauren V Collen, Scott B Snapper

Open access · bronzeAbstract readReview
In one paragraph

Review in Inflammatory bowel diseases, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed, 1 pooled it
2.6field-weighted citation impact, top 10% of its field
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

11 citing papers in PubMed, 1 synthesis or guideline pooled it, 11 citations in OpenAlex.

  1. Pooled it
  2. Nat10-mediated acScience China. Life sciences · 2026
    Article
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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

4 authors at 2 institutions in 1 country.

Jodie D OuahedDivision of Gastroenterology, Hepatology, and Nutrition, Department of Pediatrics, Boston Children's Hospital and Harvard Medical School, Boston, MA, USA.ORCID 0000-0002-2011-6209
Alexandra GriffithDivision of Gastroenterology, Hepatology, and Nutrition, Department of Pediatrics, Boston Children's Hospital and Harvard Medical School, Boston, MA, USA.
Lauren V CollenDivision of Gastroenterology, Hepatology, and Nutrition, Department of Pediatrics, Boston Children's Hospital and Harvard Medical School, Boston, MA, USA.ORCID 0000-0002-7769-8123
Scott B SnapperDivision of Gastroenterology, Hepatology, and Nutrition, Department of Pediatrics, Boston Children's Hospital and Harvard Medical School, Boston, MA, USA.
Boston Children's Hospital · USBrigham and Women's Hospital · US

Funding

STRUCTURE-FUNCTION RELATIONSHIPS IN THE ALIMENTARY TRACTP30DK034854 · NIDDK · HARVARD UNIVERSITY (MEDICAL SCHOOL) · PI JONATHAN C KAGAN · 1986 to 2026
$32.4M
Identifying Immune and Epithelial Network Signatures in Very Early Onset Inflammatory Bowel DiseaseRC2DK122532 · NIDDK · BOSTON CHILDREN'S HOSPITAL · PI KLEIN, CHRISTOPH, MUISE, ALEIXO M · 2020 to 2024
$9.1M
Role of Interferon lambda signaling in mucosal homeostasis and infantile-onset inflammatory bowel diseaseK08DK122133 · NIDDK · BOSTON CHILDREN'S HOSPITAL · PI OUAHED, JODIE · 2020 to 2024
$896k
Crohn's and Colitis Foundation Research 830997National Institute of Diabetes and Digestive Kidney Diseases of the National Institutes of Health K08DK122133National Institute of Diabetes and Digestive Kidney Diseases of the National Institutes of Health P30DK03485National Institute of Diabetes and Digestive Kidney Diseases of the National Institutes of Health RC2DK122532NIDDK NIH HHS K08 DK122133NIDDK NIH HHS P30 DK034854NIDDK NIH HHS RC2 DK122532
6 · The paper itself

Abstract

Monogenic causes of inflammatory bowel diseases (IBD) are increasingly being discovered. To date, much attention has been placed in those resulting from inborn errors of immunity. Therapeutic efforts have been largely focused on offering personalized immune modulation or curative bone marrow transplant for patients with IBD and underlying immune disorders. To date, less emphasis has been placed on monogenic causes of IBD that pertain to impairment of the intestinal epithelial barrier. Here, we provide a comprehensive review of monogenic causes of IBD that result in impaired intestinal epithelial barrier that are categorized into 6 important functions: (1) epithelial cell organization, (2) epithelial cell intrinsic functions, (3) epithelial cell apoptosis and necroptosis, (4) complement activation, (5) epithelial cell signaling, and (6) control of RNA degradation products. We illustrate how impairment of any of these categories can result in IBD. This work reviews the current understanding of the genes involved in maintaining the intestinal barrier, the inheritance patterns that result in dysfunction, features of IBD resulting from these disorders, and pertinent translational work in this field.

Indexed as

Inflammatory Bowel DiseasesIntestinal MucosaAnimalsApoptosisComplement ActivationEpithelial CellsHumansSignal Transductionhomeostasisintestinal epithelial barriermonogenic inflammatory bowel disease

Identifiers

PMID38280053
PMCPMC11519031
OpenAlexW4391276186

What OpenQuestion holds

Textmetadata
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.