Evidence map›Paper›PMID 40481471›Full record

ArticleJournal of translational medicine2025

GPR56 function as a key repressor in hepatocyte pyroptosis and the pathogenesis of liver fibrosis.

Zhemin Shi, Qi Liu, Mengxia Zhang, Xiaoxiao Du, Yifan He, Lina Zheng, Wei Hong, Tao Han, Kun Zhang

Abstract read
In one paragraph

Article in Journal of translational medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
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

2 citing papers in PubMed.

  1. [The role of hepatocyte programmed cell death in liver fibrosis].Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology · 2026
    Review
  2. Article
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.

Zhemin Shi *Department of Histology and Developmental Biology, School of Basic Medical Sciences, Tianjin Medical University, No. 22 Qixiangtai Road, Tianjin, 300070, China.
Qi Liu *Department of Histology and Developmental Biology, School of Basic Medical Sciences, Tianjin Medical University, No. 22 Qixiangtai Road, Tianjin, 300070, China.
Mengxia Zhang *Department of Histology and Developmental Biology, School of Basic Medical Sciences, Tianjin Medical University, No. 22 Qixiangtai Road, Tianjin, 300070, China.
Xiaoxiao Du *Department of Histology and Developmental Biology, School of Basic Medical Sciences, Tianjin Medical University, No. 22 Qixiangtai Road, Tianjin, 300070, China.
Yifan HeDepartment of Histology and Developmental Biology, School of Basic Medical Sciences, Tianjin Medical University, No. 22 Qixiangtai Road, Tianjin, 300070, China.
Lina ZhengDepartment of Histology and Developmental Biology, School of Basic Medical Sciences, Tianjin Medical University, No. 22 Qixiangtai Road, Tianjin, 300070, China.
Wei HongDepartment of Histology and Developmental Biology, School of Basic Medical Sciences, Tianjin Medical University, No. 22 Qixiangtai Road, Tianjin, 300070, China. hongwei@tmu.edu.cn.
Tao HanDepartment of Hepatology and Gastroenterology, Tianjin Union Medical Center, Tianjin Medical University, Tianjin Union Medical Center Affiliated to Nankai University, No. 190 Jieyuan Road, Tianjin, 300121, China. hantaomd@126.com.
Kun ZhangDepartment of Histology and Developmental Biology, School of Basic Medical Sciences, Tianjin Medical University, No. 22 Qixiangtai Road, Tianjin, 300070, China. zhangkun@tmu.edu.cn.ORCID 0000-0002-8916-556X

Funding

National Natural Science Foundation of China 32171125National Natural Science Foundation of China 32200938National Natural Science Foundation of China 81971331National Natural Science Foundation of China 82170630National Natural Science Foundation of China 82470660Natural Science Foundation of Tianjin Municipality 22JCZDJC00520Natural Science Foundation of Tianjin Municipality 23JCQNJC00400
6 · The paper itself

Abstract

backgroundGiven the rising prevalence of liver fibrosis, there is an urgent need to improve the effective diagnostic methods and treatment of liver fibrosis. Although GPCRs are involved in various physiological and pathological processes, however, the hepatic functions of GPR56 have rarely been explored. This study aims to investigate the role and underlying mechanisms of GPR56 in liver fibrosis.

methodsThe expression of GPR56 in carbon tetrachloride (CCl

resultsGPR56 was upregulated in both human and mouse fibrotic liver tissues, as well as hepatocytes from CCl

conclusionsOur study identify GPR56 as a suppressor of hepatocyte pyroptosis and liver fibrosis, underscoring its potential as a therapeutic and diagnostic target.

Indexed as

HepatocytesLiver CirrhosisPyroptosisReceptors, G-Protein-CoupledAnimalsCarbon TetrachlorideHumansMaleMiceMice, Inbred C57BLNLR Family, Pyrin Domain-Containing 3 ProteinSignal TransductionUp-RegulationCarbon TetrachlorideNLR Family, Pyrin Domain-Containing 3 ProteinReceptors, G-Protein-CoupledGPCRHepatic stellate cellsHepatocytesLiver fibrosisNF-κBPyroptosis

Identifiers

PMID40481471
PMCPMC12144805

What OpenQuestion holds

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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.