Evidence map›Paper›PMID 28279656›Full record

ArticleThe American journal of pathology2017

Hepatic Induction of Fatty Acid Binding Protein 4 Plays a Pathogenic Role in Sepsis in Mice.

Bingfang Hu, Yujin Li, Li Gao, Yan Guo, Yiwen Zhang, Xiaojuan Chai, Meishu Xu, Jiong Yan, Peipei Lu, Songrong Ren and 4 more

Open access · bronzeAbstract read
In one paragraph

Article in The American journal of pathology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.2field-weighted citation impact, top 23% 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

14 citing papers in PubMed, 35 citations in OpenAlex.

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  13. FABP4 regulates eosinophil recruitment and activation in allergic airway inflammation.American journal of physiology. Lung cellular and molecular physiology · 2018
    Article
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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 at 4 institutions in 2 countries.

Bingfang HuInstitute of Clinical Pharmacology and Guangdong Provincial Key Laboratory of New Drug Design and Evaluation, Sun Yat-Sen University, Guangzhou, China; Department of Pharmaceutical Sciences, Center for Pharmacogenetics, University of Pittsburgh, Pittsburgh, Pennsylvania.
Yujin LiInstitute of Clinical Pharmacology and Guangdong Provincial Key Laboratory of New Drug Design and Evaluation, Sun Yat-Sen University, Guangzhou, China.
Li GaoDepartment of Pharmaceutical Sciences, Center for Pharmacogenetics, University of Pittsburgh, Pittsburgh, Pennsylvania; Department of Gastroenterology, Peking University People's Hospital, Beijing, China.
Yan GuoDepartment of Pharmaceutical Sciences, Center for Pharmacogenetics, University of Pittsburgh, Pittsburgh, Pennsylvania; Department of Pathology, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Yiwen ZhangInstitute of Clinical Pharmacology and Guangdong Provincial Key Laboratory of New Drug Design and Evaluation, Sun Yat-Sen University, Guangzhou, China.
Xiaojuan ChaiDepartment of Pharmaceutical Sciences, Center for Pharmacogenetics, University of Pittsburgh, Pittsburgh, Pennsylvania; Department of Pharmaceutical Analysis and Drug Metabolism, Zhejiang Province Key Laboratory of Anti-Cancer Drug Research, College of Pharmaceutical Sciences, Zhejiang University, Hangzhou, China.
Meishu XuDepartment of Pharmaceutical Sciences, Center for Pharmacogenetics, University of Pittsburgh, Pittsburgh, Pennsylvania.
Jiong YanDepartment of Pharmaceutical Sciences, Center for Pharmacogenetics, University of Pittsburgh, Pittsburgh, Pennsylvania.
Peipei LuDepartment of Pharmaceutical Sciences, Center for Pharmacogenetics, University of Pittsburgh, Pittsburgh, Pennsylvania.
Songrong RenDepartment of Pharmaceutical Sciences, Center for Pharmacogenetics, University of Pittsburgh, Pittsburgh, Pennsylvania.
Su ZengDepartment of Pharmaceutical Analysis and Drug Metabolism, Zhejiang Province Key Laboratory of Anti-Cancer Drug Research, College of Pharmaceutical Sciences, Zhejiang University, Hangzhou, China.
Yulan LiuDepartment of Pharmaceutical Sciences, Center for Pharmacogenetics, University of Pittsburgh, Pittsburgh, Pennsylvania; Department of Gastroenterology, Peking University People's Hospital, Beijing, China.
Wen XieDepartment of Pharmaceutical Sciences, Center for Pharmacogenetics, University of Pittsburgh, Pittsburgh, Pennsylvania; Department of Pharmacology and Chemical Biology, University of Pittsburgh, Pittsburgh, Pennsylvania. Electronic address: wex6@pitt.edu.
Min HuangInstitute of Clinical Pharmacology and Guangdong Provincial Key Laboratory of New Drug Design and Evaluation, Sun Yat-Sen University, Guangzhou, China. Electronic address: huangmin@mail.sysu.edu.cn.
University of Pittsburgh · USSun Yat-sen University · CNPeking University People's Hospital · CNZhejiang University · CN

Funding

A Novel Regulation of the Phase II Enzyme Estrogen SulfotransferaseR01ES023438 · NIEHS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI XIE, WEN · 2014 to 2018
$1.7M
NIEHS NIH HHS R01 ES023438
6 · The paper itself

Abstract

Sepsis is defined as the host's deleterious systemic inflammatory response to microbial infections. Herein, we report an essential role of the fatty acid binding protein 4 (FABP4; alias adipocyte protein 2 or aP2), a lipid-binding chaperone, in sepsis response. Bioinformatic analysis of the Gene Expression Omnibus data sets showed the level of FABP4 was higher in the nonsurvival sepsis patients' whole blood compared to the survival cohorts. The expression of Fabp4 was induced in a liver-specific manner in cecal ligation and puncture (CLP) and lipopolysaccharide treatment models of sepsis. The induction of Fabp4 may have played a pathogenic role, because ectopic expression of Fabp4 in the liver sensitized mice to CLP-induced inflammatory response and worsened the animal's survival. In contrast, pharmacological inhibition of Fabp4 markedly alleviated the CLP responsive inflammation and tissue damage and improved survival. We conclude that FABP4 is an important mediator of the sepsis response. Early intervention by pharmacological inhibition of FABP4 may help to manage sepsis in the clinic.

Indexed as

Adipose TissueAnimalsCecumDisease Models, AnimalEscherichia coli InfectionsFatty Acid-Binding ProteinsFemaleHepatocytesHumansInterleukin-6Kupffer CellsLigationLipopolysaccharidesLiverMiceMice, Inbred C57BLFABP4 protein, humanFabp4 protein, mouseFatty Acid-Binding ProteinsInterleukin-6LipopolysaccharidesPimozide

Identifiers

PMID28279656
PMCPMC5417005
OpenAlexW2593086035

What OpenQuestion holds

Textmetadata
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.