Evidence map›Paper›PMID 34911928›Full record

ArticleCell death & disease2021

GPR120 induces regulatory dendritic cells by inhibiting HK2-dependent glycolysis to alleviate fulminant hepatic failure.

Hongshuang Yu, Wanlin Yang, Jiefang Huang, Xiang Miao, Bei Wang, Xiaohui Ren, Yuting Gu, Qiwei Wang, Xinyuan Ding, Xin Guo and 5 more

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
3.0field-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

10 citing papers in PubMed, 46 citations in OpenAlex.

  1. S100A10 promotes glycolysis and malignant progression of CCA by activating the HK2/ERK signaling pathway.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026
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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

15 authors at 4 institutions in 1 country.

Hongshuang Yu *Clinical Research Centre, The Affiliated Changshu Hospital of Xuzhou Medical University, Changshu, China.
Wanlin Yang *Children's Hospital of Soochow University, Institutes for Translational Medicine, State Key Laboratory of Radiation Medicine and Protection, Key Laboratory of Stem Cells and Medical Biomaterials of Jiangsu Province, Medical College of Soochow University, Soochow University, Suzhou, Jiangsu, China.
Jiefang HuangClinical Research Centre, The Affiliated Changshu Hospital of Xuzhou Medical University, Changshu, China.
Xiang MiaoShanghai Institute of Nutrition and Health, Shanghai Institutes for Biological Sciences, University of Chinese Academy of Sciences, Chinese Academy of Sciences, Shanghai, China.
Bei WangShanghai Institute of Nutrition and Health, Shanghai Institutes for Biological Sciences, University of Chinese Academy of Sciences, Chinese Academy of Sciences, Shanghai, China.
Xiaohui RenShanghai Institute of Nutrition and Health, Shanghai Institutes for Biological Sciences, University of Chinese Academy of Sciences, Chinese Academy of Sciences, Shanghai, China.
Yuting GuDepartment of Stomatology, Renji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China.
Qiwei WangShanghai Institute of Nutrition and Health, Shanghai Institutes for Biological Sciences, University of Chinese Academy of Sciences, Chinese Academy of Sciences, Shanghai, China.
Xinyuan DingChildren's Hospital of Soochow University, Institutes for Translational Medicine, State Key Laboratory of Radiation Medicine and Protection, Key Laboratory of Stem Cells and Medical Biomaterials of Jiangsu Province, Medical College of Soochow University, Soochow University, Suzhou, Jiangsu, China.
Xin GuoChildren's Hospital of Soochow University, Institutes for Translational Medicine, State Key Laboratory of Radiation Medicine and Protection, Key Laboratory of Stem Cells and Medical Biomaterials of Jiangsu Province, Medical College of Soochow University, Soochow University, Suzhou, Jiangsu, China.
Fengtao QianShanghai Institute of Nutrition and Health, Shanghai Institutes for Biological Sciences, University of Chinese Academy of Sciences, Chinese Academy of Sciences, Shanghai, China.
Yanyun ZhangClinical Research Centre, The Affiliated Changshu Hospital of Xuzhou Medical University, Changshu, China.
Huanbai XuDepartment of Endocrinology and Metabolism, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China. huanbaixu@126.com.ORCID http://orcid.org/0000-0002-4294-0274
Leizhen ZhengDepartment of Oncology, Xinhua Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China. zhengleizhen@xinhuamed.com.cn.ORCID http://orcid.org/0000-0003-1309-3755
Min JinClinical Research Centre, The Affiliated Changshu Hospital of Xuzhou Medical University, Changshu, China. mjin@sibs.ac.cn.ORCID http://orcid.org/0000-0003-0073-4816
Shanghai Institute of Nutrition and Health · CNXuzhou Medical College · CNShanghai Jiao Tong University · CNSoochow University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Fulminant hepatic failure (FHF) is a potentially fatal liver disease that is associated with intrahepatic infiltration of inflammatory cells. As the receptor of polyunsaturated long chain fatty acids, GPR120 can regulate cell differentiation, proliferation, metabolism, and immune response. However, whether GPR120 is involved in FHF remains unknown. Using Propionibacterium acnes (P. acnes)-primed, LPS-induced FHF in mice, we found that interference with GPR120 activity using pharmacological agonist attenuated the severity of the liver injury and mortality of FHF in mice, while a lack of GPR120 exacerbated the disease. GPR120 activation potently alleviated FHF and led to decreased T helper (Th) 1 cell response and expansion of regulatory T cells (Tregs). Interestingly, GPR120 agonist didn't directly target T cells, but dramatically induced a distinct population of CD11c

Indexed as

AnimalsCase-Control StudiesDendritic CellsDisease Models, AnimalFemaleGlycolysisHumansLiver Failure, AcuteMiceReceptors, G-Protein-CoupledFFAR4 protein, mouseReceptors, G-Protein-Coupled

Identifiers

PMID34911928
PMCPMC8674251
OpenAlexW4200131182

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.