Evidence map›Paper›PMID 38982366›Full record

ArticleMolecular medicine (Cambridge, Mass.)2024

Deletion of GPR81 activates CREB/Smad7 pathway and alleviates liver fibrosis in mice.

Ying Zhi, Kerui Fan, Shuang Liu, Kai Hu, Xinyan Zan, Ling Lin, Yongqiang Yang, Xianqiong Gong, Kun Chen, Li Tang and 4 more

Abstract read
In one paragraph

Article in Molecular medicine (Cambridge, Mass.), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing 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

13 citing papers in PubMed.

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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

14 authors.

Ying Zhi *Department of Pathophysiology, Basic Medical College, Chongqing Medical University, 1 Yixueyuan Road, Chongqing, 400016, China.
Kerui Fan *Laboratory of Stem Cell and Tissue Engineering, Chongqing Medical University, Chongqing, China.
Shuang Liu *Department of Pathophysiology, Basic Medical College, Chongqing Medical University, 1 Yixueyuan Road, Chongqing, 400016, China.
Kai HuDepartment of Pathophysiology, Basic Medical College, Chongqing Medical University, 1 Yixueyuan Road, Chongqing, 400016, China.
Xinyan ZanDepartment of Pathophysiology, Basic Medical College, Chongqing Medical University, 1 Yixueyuan Road, Chongqing, 400016, China.
Ling LinDepartment of Pathophysiology, Basic Medical College, Chongqing Medical University, 1 Yixueyuan Road, Chongqing, 400016, China.
Yongqiang YangDepartment of Pathophysiology, Basic Medical College, Chongqing Medical University, 1 Yixueyuan Road, Chongqing, 400016, China.
Xianqiong GongHepatology Center, Xiamen Hospital of Traditional Chinese Medicine, Xiamen, Fujian, China.
Kun ChenDepartment of Pathophysiology, Basic Medical College, Chongqing Medical University, 1 Yixueyuan Road, Chongqing, 400016, China.
Li TangDepartment of Pathophysiology, Basic Medical College, Chongqing Medical University, 1 Yixueyuan Road, Chongqing, 400016, China.
Longjiang LiDepartment of Pathophysiology, Basic Medical College, Chongqing Medical University, 1 Yixueyuan Road, Chongqing, 400016, China.
Jiayi HuangDepartment of Pathophysiology, Basic Medical College, Chongqing Medical University, 1 Yixueyuan Road, Chongqing, 400016, China.
Shujun ZhangChongqing Key Laboratory of Infectious Diseases and Parasitic Diseases, Department of Infectious Diseases, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China. sjzhang@hospital.cqmu.edu.cn.
Li ZhangDepartment of Pathophysiology, Basic Medical College, Chongqing Medical University, 1 Yixueyuan Road, Chongqing, 400016, China. zhangli@cqmu.edu.cn.ORCID 0000-0001-7503-6567

Funding

Natural Science Foundation of Chongqing No. CSTB2022NSCQ-MSX1077Xiamen Science and Technology Plan Project No. 3502Z20224020
6 · The paper itself

Abstract

backgroundEnhanced glycolysis is a crucial metabolic event that drives the development of liver fibrosis, but the molecular mechanisms have not been fully understood. Lactate is the endproduct of glycolysis, which has recently been identified as a bioactive metabolite binding to G-protein-coupled receptor 81 (GPR81). We then questioned whether GPR81 is implicated in the development of liver fibrosis.

methodsThe level of GPR81 was determined in mice with carbon tetrachloride (CCl

resultsCCl

conclusionGPR81 might be a detrimental factor that promotes the development of liver fibrosis by regulating CREB/Smad7 pathway.

Indexed as

Carbon TetrachlorideCyclic AMP Response Element-Binding ProteinHepatic Stellate CellsLiver CirrhosisMice, KnockoutReceptors, G-Protein-CoupledSignal TransductionSmad7 ProteinAnimalsCell LineDisease Models, AnimalGene DeletionHumansMaleMiceMice, Inbred C57BLCarbon TetrachlorideCreb1 protein, mouseCyclic AMP Response Element-Binding ProteinHcar1 protein, mouseReceptors, G-Protein-CoupledSmad7 ProteinSmad7 protein, mouseTransforming Growth Factor beta1cAMPCREBG-protein-coupled receptor 81Liver fibrosisSmad7

Identifiers

PMID38982366
PMCPMC11234765

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

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.