Evidence map›Paper›PMID 34124180›Full record

ArticleInflammatory intestinal diseases2021

Hypoxia Reduces the Transcription of Fibrotic Markers in the Intestinal Mucosa.

Simona Simmen, Max Maane, Sarah Rogler, Katherina Baebler, Silvia Lang, Jesus Cosin-Roger, Kirstin Atrott, Isabelle Frey-Wagner, Partick Spielmann, Roland H Wenger and 7 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Inflammatory intestinal diseases, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.3field-weighted citation impact, top 54% 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

3 citing papers in PubMed, 5 citations in OpenAlex.

  1. Review
  2. Review
  3. 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

17 authors at 1 institution in 1 country.

Simona SimmenDepartment of Gastroenterology and Hepatology, University of Zurich, Zurich, Switzerland.
Max MaaneDepartment of Gastroenterology and Hepatology, University of Zurich, Zurich, Switzerland.
Sarah RoglerDepartment of Gastroenterology and Hepatology, University of Zurich, Zurich, Switzerland.
Katherina BaeblerDepartment of Gastroenterology and Hepatology, University of Zurich, Zurich, Switzerland.
Silvia LangDepartment of Gastroenterology and Hepatology, University of Zurich, Zurich, Switzerland.
Jesus Cosin-RogerDepartment of Gastroenterology and Hepatology, University of Zurich, Zurich, Switzerland.
Kirstin AtrottDepartment of Gastroenterology and Hepatology, University of Zurich, Zurich, Switzerland.
Isabelle Frey-WagnerDepartment of Gastroenterology and Hepatology, University of Zurich, Zurich, Switzerland.
Partick SpielmannInstitute of Physiology, University of Zurich, Zurich, Switzerland.
Roland H WengerInstitute of Physiology, University of Zurich, Zurich, Switzerland.
Bruce WederDepartment of Gastroenterology and Hepatology, University of Zurich, Zurich, Switzerland.
Jonas ZeitzDepartment of Gastroenterology and Hepatology, University of Zurich, Zurich, Switzerland.
Stephan R VavrickaDepartment of Gastroenterology and Hepatology, University of Zurich, Zurich, Switzerland.
Gerhard RoglerDepartment of Gastroenterology and Hepatology, University of Zurich, Zurich, Switzerland.
Cheryl de VallièreDepartment of Gastroenterology and Hepatology, University of Zurich, Zurich, Switzerland.
Martin HausmannDepartment of Gastroenterology and Hepatology, University of Zurich, Zurich, Switzerland.
Pedro A RuizDepartment of Gastroenterology and Hepatology, University of Zurich, Zurich, Switzerland.
University of Zurich · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionIntestinal fibrosis, characterized by excessive deposition of extracellular matrix proteins, is a common and severe clinical complication of inflammatory bowel disease (IBD). However, the mechanisms underlying fibrosis remain elusive, and currently, there are limited effective pharmacologic treatments that target the development of fibrosis. Hypoxia is one of the key microenvironmental factors influencing intestinal inflammation and has been linked to fibrosis.

objectiveIn the present study, we sought to elucidate the impact of hypoxia on fibrotic gene expression in the intestinal mucosa.

methodsHuman volunteers, IBD patients, and dextran sulphate sodium-treated mice were exposed to hypoxia, and colonic biopsies were collected. The human intestinal epithelial cell line Caco-2, human THP-1 macrophages, and primary human gut fibroblasts were subjected to hypoxia, and changes in fibrotic gene expression were assessed.

resultsHuman volunteers subjected to hypoxia presented reduced transcriptional levels of fibrotic and epithelial-mesenchymal transition markers in the intestinal mucosa. IBD patients showed a trend towards a decrease in tissue inhibitor of metalloproteinase 1 protein expression. In mice, hypoxic conditions reduced the colonic expression of several collagens and matrix metalloproteinases. Hypoxic Caco-2 cells, THP-1 cells, and primary gut fibroblasts showed a significant downregulation in the expression of fibrotic and tissue remodelling factors.

conclusionsStabilization of hypoxia-inducible factors might represent a novel therapeutic approach for the treatment of IBD-associated fibrosis.

Indexed as

Epithelial-mesenchymal transitionGut fibroblastsInflammatory bowel diseasesIntestinal epithelial cellsWound healing

Identifiers

PMID34124180
PMCPMC8160569
OpenAlexW3145369816

What OpenQuestion holds

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Registered trials

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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.