Evidence map›Paper›PMID 30611442›Full record

ReviewMayo Clinic proceedings2019

Mechanisms of Disease: Inflammatory Bowel Diseases.

Guilherme Piovezani Ramos, Konstantinos A Papadakis

Abstract readReview
In one paragraph

Review in Mayo Clinic proceedings, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 532 papers, 7 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
532citing papers in PubMed, 7 pooled it
69.0field-weighted citation impact, top 1% 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

532 citing papers in PubMed, 7 syntheses or guidelines pooled it, 968 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Pooled it
  5. Pooled it
  6. Pooled it
  7. Pooled it
  8. Inflammatory bowel disease and breast cancer: epidemiological evidence, shared biology, and clinical management.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
    Review
  9. Review
  10. Anti-inflammatory activity of Chlorella polysaccharide AHP.Molecular and cellular biochemistry · 2026
    Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Article
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  19. Review
  20. Ryanodine Receptor 1 Is Dispensable for CD4European journal of immunology · 2026
    Article

472 more citing papers are in PubMed but not listed here.

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

2 authors at 1 institution in 1 country.

Guilherme Piovezani RamosDepartment of Internal Medicine, Mayo Clinic, Rochester, MN; Division of Gastroenterology and Hepatology, Mayo Clinic, Rochester, MN.
Konstantinos A PapadakisDivision of Gastroenterology and Hepatology, Mayo Clinic, Rochester, MN. Electronic address: Papadakis.konstantinos@mayo.edu.
Mayo Clinic in Arizona · US

Funding

Kruppel-like factor (KLF) 10 regulates intestinal macrophages and experimental colitisR03AI131011 · NIAID · MAYO CLINIC ROCHESTER · PI PAPADAKIS, KONSTANTINOS A · 2018 to 2019
$159k
NIAID NIH HHS R03 AI131011
6 · The paper itself

Abstract

Inflammatory bowel diseases (IBDs), represented by Crohn disease and ulcerative colitis, are associated with major morbidity in Western countries and with increasing incidence in the developing world. Although analysis of the genome of patients with IBD, especially through genome-wide association studies, has unraveled multiple pathways involved in IBD pathogenesis, only part of IBD heritability has been explained by genetic studies. This finding has revealed that environmental factors also play a major role in promoting intestinal inflammation, mostly through their effects in the composition of the microbiome. However, in order for microbial dysbiosis to result in uncontrolled intestinal inflammation, the intestinal barrier formed by intestinal epithelial cells and the innate immune system should also be compromised. Finally, activation of the immune system depends on the working balance between effector and regulatory cells present in the intestinal mucosa, which have also been found to be dysregulated in this patient population. Therefore, IBD pathogenesis is a result of the interplay of genetic susceptibility and environmental impact on the microbiome that through a weakened intestinal barrier will lead to inappropriate intestinal immune activation. In this article, we will review the mechanisms proposed to cause IBD from the genetic, environmental, intestinal barrier, and immunologic perspectives.

Indexed as

Genetic Predisposition to DiseaseGenome-Wide Association StudyHumansInflammatory Bowel DiseasesIntestinal Mucosa

Identifiers

PMID30611442
PMCPMC6386158
OpenAlexW2906727442

What OpenQuestion holds

Textmetadata
LicenceTDM
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.