Evidence map›Paper›PMID 26696888›Full record

ArticleFrontiers in pharmacology2015

The G-Protein-Coupled Bile Acid Receptor Gpbar1 (TGR5) Inhibits Gastric Inflammation Through Antagonizing NF-κB Signaling Pathway.

Cong Guo, Hui Qi, Yingjie Yu, Qiqi Zhang, Jia Su, Donna Yu, Wendong Huang, Wei-Dong Chen, Yan-Dong Wang

Open access · goldAbstract read
In one paragraph

Article in Frontiers in pharmacology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed
3.2field-weighted citation impact, top 6% 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

48 citing papers in PubMed, 88 citations in OpenAlex.

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  12. Annals of translational medicine · 2022
    Article
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  15. The role of bile acids in carcinogenesis.Cellular and molecular life sciences : CMLS · 2022
    Review
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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

9 authors at 5 institutions in 2 countries.

Cong GuoState Key Laboratory of Chemical Resource Engineering, College of Life Science and Technology, Beijing University of Chemical Technology Beijing, China.
Hui QiKey Laboratory of Receptors-Mediated Gene Regulation and Drug Discovery, School of Medicine, Henan University Kaifeng, China ; Key Laboratory of Molecular Pathology, School of Basic Medical Science, Inner Mongolia Medical University Hohhot, China.
Yingjie YuDepartment of Materials Science and Engineering, State University of New York at Stony Brook Stony Brook, NY, USA.
Qiqi ZhangState Key Laboratory of Chemical Resource Engineering, College of Life Science and Technology, Beijing University of Chemical Technology Beijing, China.
Jia SuState Key Laboratory of Chemical Resource Engineering, College of Life Science and Technology, Beijing University of Chemical Technology Beijing, China.
Donna YuDepartment of Diabetes and Metabolic Diseases Research, Beckman Research Institute, City of Hope National Medical Center Duarte, CA, USA.
Wendong HuangDepartment of Diabetes and Metabolic Diseases Research, Beckman Research Institute, City of Hope National Medical Center Duarte, CA, USA.
Wei-Dong ChenKey Laboratory of Receptors-Mediated Gene Regulation and Drug Discovery, School of Medicine, Henan University Kaifeng, China ; Key Laboratory of Molecular Pathology, School of Basic Medical Science, Inner Mongolia Medical University Hohhot, China.
Yan-Dong WangState Key Laboratory of Chemical Resource Engineering, College of Life Science and Technology, Beijing University of Chemical Technology Beijing, China.
Beijing University of Chemical Technology · CNCity Of Hope National Medical Center · USHenan University · CNInner Mongolia Medical University · CNStony Brook University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Gpbar1 (TGR5), a membrane-bound bile acid receptor, is well-known for its roles in regulation of energy homeostasis and glucose metabolism. Here, we show that mice lacking TGR5 were much more susceptible to lipopolysaccharide (LPS)-induced acute gastric inflammation than wild-type (WT) mice and TGR5 is a negative regulator of gastric inflammation through antagonizing NF-κB signaling pathway. We found that the treatment of TGR5 ligands 23(S)-mCDCA and GPBARA (3-(2-Chlorophenyl)-N-(4-chlorophenyl)-N,5-dimethylisoxazole-4-carboxamide) suppressed gene and protein expression mediated by NF-κB signaling. TGR5 overexpression with ligand treatment inhibited gene expression of interferon-inducible protein 10 (IP-10), TNF-α, and chemoattractant protein-1 (MCP-1) induced by LPS. Furthermore, we revealed that TGR5 activation antagonized NF-κB signaling pathway through suppressing its transcription activity, the phosphorylation of IκBα and p65 translocation, which suggests that TGR5 antagonizes gastric inflammation at least in part by inhibiting NF-κB signaling. These findings identify TGR5 as a negative mediator of gastric inflammation that may serve as an attractive therapeutic tool for human gastric inflammation and cancer.

Indexed as

gastric inflammationGPBAR1GPCRNF-κBtgr5

Identifiers

PMID26696888
PMCPMC4675858
OpenAlexW2191241037

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.