Evidence map›Paper›PMID 33519819›Full record

ArticleFrontiers in immunology2020

Local Stabilization of Hypoxia-Inducible Factor-1α Controls Intestinal Inflammation

Young-In Kim, Eun-Je Yi, Young-Dae Kim, A Reum Lee, Jiwoung Chung, Hae Chan Ha, Joong Myung Cho, Seong-Ryeol Kim, Hyun-Jeong Ko, Jae-Hee Cheon and 2 more

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
3.7field-weighted citation impact, top 5% 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

36 citing papers in PubMed, 50 citations in OpenAlex.

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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

12 authors at 4 institutions in 1 country.

Young-In KimLaboratory of Microbiology, College of Pharmacy and Research Institute of Pharmaceutical Science and Technology, Ajou University, Suwon, South Korea.
Eun-Je YiLaboratory of Microbiology, College of Pharmacy and Research Institute of Pharmaceutical Science and Technology, Ajou University, Suwon, South Korea.
Young-Dae KimInstitute for Drug Discovery, CrystalGenomics, Inc., Seongnam-si, South Korea.
A Reum LeeInstitute for Drug Discovery, CrystalGenomics, Inc., Seongnam-si, South Korea.
Jiwoung ChungInstitute for Drug Discovery, CrystalGenomics, Inc., Seongnam-si, South Korea.
Hae Chan HaInstitute for Drug Discovery, CrystalGenomics, Inc., Seongnam-si, South Korea.
Joong Myung ChoInstitute for Drug Discovery, CrystalGenomics, Inc., Seongnam-si, South Korea.
Seong-Ryeol KimLaboratory of Microbiology and Immunology, Department of Pharmacy, Kangwon National University, Chuncheon-si, South Korea.
Hyun-Jeong KoLaboratory of Microbiology and Immunology, Department of Pharmacy, Kangwon National University, Chuncheon-si, South Korea.
Jae-Hee CheonDepartment of Internal Medicine and Institute of Gastroenterology, Yonsei University College of Medicine, Seoul, South Korea.
Yong Rae HongInstitute for Drug Discovery, CrystalGenomics, Inc., Seongnam-si, South Korea.
Sun-Young ChangLaboratory of Microbiology, College of Pharmacy and Research Institute of Pharmaceutical Science and Technology, Ajou University, Suwon, South Korea.
CrystalGenomics (South Korea) · KRAjou University · KRKangwon National University · KRYonsei University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Intestinal epithelial cells are adapted in mucosal hypoxia and hypoxia-inducible factors in these cells can fortify barrier integrity to support mucosal tissue healing. Here we investigated whether hypoxia-related pathways could be proposed as potential therapeutic targets for inflammatory bowel disease. We developed a novel hypoxia-inducible factor (HIF) prolyl hydroxylase inhibitor, CG-598 which stabilized HIF-1α in the gut tissue. Treatment of CG-598 did not affect extra-intestinal organs or cause any significant adverse effects such as erythropoiesis. In the experimental murine colitis model, CG-598 ameliorated intestinal inflammation with reduction of inflammatory lesions and pro-inflammatory cytokines. CG-598 treatment fortified barrier function by increasing the expression of intestinal trefoil factor, CD73, E-cadherin and mucin. Also, IL-10 and IL-22 were induced from lamina propria CD4

Indexed as

AnimalsCaco-2 CellsCell Line, TumorColitisCytokinesDisease Models, AnimalFemaleHCT116 CellsHeLa CellsHumansHypoxiaHypoxia-Inducible Factor 1, alpha SubunitInflammationInflammatory Bowel DiseasesIntestinal MucosaMaleCytokinesHIF1A protein, humanHypoxia-Inducible Factor 1, alpha SubunitProlyl-Hydroxylase InhibitorsTrefoil Factor-3gut barrierhypoxia-inducible factorimmune regulationinflammatory bowel diseaseprolyl hydroxylase inhibitor

Identifiers

PMID33519819
PMCPMC7840603
OpenAlexW3119118230

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.