Evidence map›Paper›PMID 37837511›Full record

SynthesisUnited European gastroenterology journal2024

ATG16L1 rs2241880/T300A increases susceptibility to perianal Crohn's disease: An updated meta-analysis on inflammatory bowel disease risk and clinical outcomes.

Isidora Simovic, Ida Hilmi, Ruey Terng Ng, Kee Seang Chew, Shin Yee Wong, Way Seah Lee, Stephen Riordan, Natalia Castaño-Rodríguez

Open access · hybridAbstract readMeta-Analysis
In one paragraph

Synthesis in United European gastroenterology journal, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed, 3 pooled it
3.4field-weighted citation impact, top 7% 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

12 citing papers in PubMed, 3 syntheses or guidelines pooled it, 11 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Review
  5. Review
  6. Article
  7. Review
  8. Review
  9. Article
  10. Article
  11. Review
  12. Review
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

8 authors at 3 institutions in 3 countries.

Isidora SimovicSchool of Biotechnology and Biomolecular Sciences, UNSW Sydney, Sydney, New South Wales, Australia.
Ida HilmiDepartment of Medicine, Faculty of Medicine, University Malaya, Kuala Lumpur, Malaysia.
Ruey Terng NgDepartment of Paediatrics, Faculty of Medicine, University Malaya, Kuala Lumpur, Malaysia.
Kee Seang ChewDepartment of Paediatrics, Faculty of Medicine, University Malaya, Kuala Lumpur, Malaysia.
Shin Yee WongDepartment of Paediatrics, Faculty of Medicine, University Malaya, Kuala Lumpur, Malaysia.
Way Seah LeeDepartment of Paediatrics, Faculty of Medicine, University Malaya, Kuala Lumpur, Malaysia.
Stephen RiordanPrince of Wales Clinical School, Faculty of Medicine, University of New South Wales, Kuala Lumpur, Malaysia.
Natalia Castaño-RodríguezSchool of Biotechnology and Biomolecular Sciences, UNSW Sydney, Sydney, New South Wales, Australia.ORCID 0000-0001-8819-8872
University of Malaya · MYUNSW Sydney · AUPrince of Wales Hospital · CN

Funding

Australian Government Australian Government Research Training Programme ScCancer Australia PdCCRS Early Career Researcher Grant (2012944)Cancer Institute NSW Early Career Fellowship (2019/ECF1082)Pancare Foundation PdCCRS Early Career Researcher Grant (2012944)Universiti Malaya UM.C/625/HIR/MOHE/CHAN/13/1University of New South Wales Scientia Fellowship
6 · The paper itself

Abstract

backgroundATG16L1 plays a fundamental role in the degradative intracellular pathway known as autophagy, being a mediator of inflammation and microbial homeostasis. The variant rs2241880 can diminish these capabilities, potentially contributing to inflammatory bowel disease (IBD) pathogenesis.

objectivesTo perform an updated meta-analysis on the association between ATG16L1 rs2241880 and IBD susceptibility by exploring the impact of age, ethnicity, and geography. Moreover, to investigate the association between rs2241880 and clinical features.

methodsLiterature searches up until September 2022 across 7 electronic public databases were performed for all case-control studies on ATG16L1 rs2241880 and IBD. Pooled odds ratios (OR

resultsOur analyses included a total of 30,606 IBD patients, comprising 21,270 Crohn's disease (CD) and 9336 ulcerative colitis (UC) patients, and 33,329 controls. ATG16L1 rs2241880 was significantly associated with CD susceptibility, where the A allele was protective (OR

conclusionsATG16L1 rs2241880 (G allele) is a consistent risk factor for IBD in Caucasian cohorts and influences clinical outcomes. As its role in non-Caucasian populations remains ambiguous, further studies in under-reported populations are necessary.

Indexed as

Crohn DiseaseInflammatory Bowel DiseasesAutophagy-Related ProteinsCarrier ProteinsGenetic Predisposition to DiseaseGenotypeHumansPolymorphism, Single NucleotideATG16L1 protein, humanAutophagy-Related ProteinsCarrier ProteinsATG16L1autophagybiomarkerCrohn diseaseIBDinflammatory bowel diseaseperianalrisk factorrs2241880ulcerative colitis

Identifiers

PMID37837511
PMCPMC10859713
OpenAlexW4387639463

What OpenQuestion holds

Textmetadata
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.