Evidence map›Paper›PMID 38001521›Full record

ArticleMilitary Medical Research2023

Targeting GPR65 alleviates hepatic inflammation and fibrosis by suppressing the JNK and NF-κB pathways.

Kun Zhang, Meng-Xia Zhang, Xiao-Xiang Meng, Jing Zhu, Jia-Jun Wang, Yi-Fan He, Ye-Hua Li, Si-Cong Zhao, Zhe-Min Shi, Li-Na Zheng and 2 more

Open access · diamondAbstract read
In one paragraph

Article in Military Medical Research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed
6.3field-weighted citation impact, top 3% 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

50 citing papers in PubMed, 41 citations in OpenAlex.

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  14. Quorum sensing geneFrontiers in microbiology · 2026
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

12 authors at 2 institutions in 1 country.

Kun Zhang *Department of Histology and Embryology, School of Basic Medical Sciences, Tianjin Medical University, Tianjin, 300070, China.
Meng-Xia Zhang *Department of Histology and Embryology, School of Basic Medical Sciences, Tianjin Medical University, Tianjin, 300070, China.
Xiao-Xiang Meng *Department of Histology and Embryology, School of Basic Medical Sciences, Tianjin Medical University, Tianjin, 300070, China.
Jing ZhuDepartment of Histology and Embryology, School of Basic Medical Sciences, Tianjin Medical University, Tianjin, 300070, China.
Jia-Jun WangDepartment of Histology and Embryology, School of Basic Medical Sciences, Tianjin Medical University, Tianjin, 300070, China.
Yi-Fan HeDepartment of Histology and Embryology, School of Basic Medical Sciences, Tianjin Medical University, Tianjin, 300070, China.
Ye-Hua LiDepartment of Histology and Embryology, School of Basic Medical Sciences, Tianjin Medical University, Tianjin, 300070, China.
Si-Cong ZhaoDepartment of Histology and Embryology, School of Basic Medical Sciences, Tianjin Medical University, Tianjin, 300070, China.
Zhe-Min ShiDepartment of Histology and Embryology, School of Basic Medical Sciences, Tianjin Medical University, Tianjin, 300070, China.
Li-Na ZhengDepartment of Histology and Embryology, School of Basic Medical Sciences, Tianjin Medical University, Tianjin, 300070, China.
Tao HanDepartment of Hepatology and Gastroenterology, Tianjin Union Medical Center, Tianjin Medical University, Tianjin Union Medical Center affiliated to Nankai University, Tianjin, 300000, China. hantaomd@126.com.
Wei HongDepartment of Histology and Embryology, School of Basic Medical Sciences, Tianjin Medical University, Tianjin, 300070, China. hongwei@tmu.edu.cn.ORCID 0000-0003-1199-4365
Tianjin Medical University · CNNankai University · CN

Funding

National Natural Science Foundation of China 32171125National Natural Science Foundation of China 81971331National Natural Science Foundation of China 82170630
6 · The paper itself

Abstract

backgroundG-protein coupled receptors (GPCRs) are recognized as attractive targets for drug therapy. However, it remains poorly understood how GPCRs, except for a few chemokine receptors, regulate the progression of liver fibrosis. Here, we aimed to reveal the role of GPR65, a proton-sensing receptor, in liver fibrosis and to elucidate the underlying mechanism.

methodsThe expression level of GPR65 was evaluated in both human and mouse fibrotic livers. Furthermore, Gpr65-deficient mice were treated with either bile duct ligation (BDL) for 21 d or carbon tetrachloride (CCl

resultsWe found that hepatic macrophages (HMs)-enriched GPR65 was upregulated in both human and mouse fibrotic livers. Moreover, knockout of Gpr65 significantly alleviated BDL- and CCl

conclusionsGPR65 is a major regulator that modulates the progression of liver fibrosis. Thus, targeting GPR65 could be an effective therapeutic strategy for the prevention of liver fibrosis.

Indexed as

Interleukin-6NF-kappa BAnimalsHumansInflammationLiver CirrhosisMiceReceptors, G-Protein-CoupledTransforming Growth Factor betaTumor Necrosis Factor-alphaGPR65 protein, humanGPR65 protein, mouseInterleukin-6NF-kappa BReceptors, G-Protein-CoupledTransforming Growth Factor betaTumor Necrosis Factor-alphaGPR65Hepatic fibrosisHepatic macrophagesInflammationJNKNF-κB

Identifiers

PMID38001521
PMCPMC10675918
OpenAlexW4388990561

What OpenQuestion holds

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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.