Evidence map›Paper›PMID 30337250›Full record

ArticleEBioMedicine2018

Noncanonical farnesoid X receptor signaling inhibits apoptosis and impedes liver fibrosis.

Hong Wang, Chaoliang Ge, Jiyu Zhou, Yitong Guo, Shuang Cui, Ningning Huang, Tingting Yan, Lijuan Cao, Yuan Che, Qiuling Zheng and 4 more

Open access · goldAbstract read
In one paragraph

Article in EBioMedicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

22 citing papers in PubMed, 50 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
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  7. Review
  8. Review
  9. Review
  10. Roles ofFrontiers in genetics · 2024
    Article
  11. Article
  12. Article
  13. Review
  14. Review
  15. Knockout of farnesoid X receptor gene aggravates cisplatin-induced kidney injury.Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2022
    Article
  16. FXR-Deoxycholic Acid-TNF-α Axis Modulates Acetaminophen-Induced Hepatotoxicity.Toxicological sciences : an official journal of the Society of Toxicology · 2021
    Article
  17. Article
  18. An Update on Efficacy and Safety of Emerging Hepatic Antifibrotic Agents.Journal of clinical and translational hepatology · 2021
    Review
  19. Liver Fibrosis: Therapeutic Targets and Advances in Drug Therapy.Frontiers in cell and developmental biology · 2021
    Review
  20. Carbon tetrachloride (CClBMC gastroenterology · 2020
    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

14 authors at 2 institutions in 2 countries.

Hong WangState Key Laboratory of Natural Medicines, Key Laboratory of Drug Metabolism and Pharmacokinetics, China Pharmaceutical University, Nanjing 210009, China.
Chaoliang GeState Key Laboratory of Natural Medicines, Key Laboratory of Drug Metabolism and Pharmacokinetics, China Pharmaceutical University, Nanjing 210009, China; Department of Pharmacy, The First Affiliated Hospital of Anhui Medical University, Hefei 230022, China.
Jiyu ZhouState Key Laboratory of Natural Medicines, Key Laboratory of Drug Metabolism and Pharmacokinetics, China Pharmaceutical University, Nanjing 210009, China.
Yitong GuoState Key Laboratory of Natural Medicines, Key Laboratory of Drug Metabolism and Pharmacokinetics, China Pharmaceutical University, Nanjing 210009, China.
Shuang CuiState Key Laboratory of Natural Medicines, Key Laboratory of Drug Metabolism and Pharmacokinetics, China Pharmaceutical University, Nanjing 210009, China.
Ningning HuangState Key Laboratory of Natural Medicines, Key Laboratory of Drug Metabolism and Pharmacokinetics, China Pharmaceutical University, Nanjing 210009, China.
Tingting YanLaboratory of Metabolism, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA.
Lijuan CaoState Key Laboratory of Natural Medicines, Key Laboratory of Drug Metabolism and Pharmacokinetics, China Pharmaceutical University, Nanjing 210009, China.
Yuan CheState Key Laboratory of Natural Medicines, Key Laboratory of Drug Metabolism and Pharmacokinetics, China Pharmaceutical University, Nanjing 210009, China.
Qiuling ZhengState Key Laboratory of Natural Medicines, Key Laboratory of Drug Metabolism and Pharmacokinetics, China Pharmaceutical University, Nanjing 210009, China.
Xiao ZhengState Key Laboratory of Natural Medicines, Key Laboratory of Drug Metabolism and Pharmacokinetics, China Pharmaceutical University, Nanjing 210009, China.
Frank J GonzalezLaboratory of Metabolism, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA.
Guangji WangState Key Laboratory of Natural Medicines, Key Laboratory of Drug Metabolism and Pharmacokinetics, China Pharmaceutical University, Nanjing 210009, China. Electronic address: gjwang@cpu.edu.cn.
Haiping HaoState Key Laboratory of Natural Medicines, Key Laboratory of Drug Metabolism and Pharmacokinetics, China Pharmaceutical University, Nanjing 210009, China. Electronic address: haipinghao@cpu.edu.cn.
China Pharmaceutical University · CNNational Institutes of Health · US

Funding

Xenobiotic ReceptorsZIABC005708 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI GONZALEZ, FRANK J · 2009 to 2025
$16.4M
6 · The paper itself

Abstract

backgroundHepatocyte is particularly vulnerable to apoptosis, a hallmark of many liver diseases. Although pro-apoptotic mechanisms have been extensively explored, less is known about the hepatocyte-specific anti-apoptotic molecular events and it lacks effective approach to combat hepatocyte apoptosis. We investigated the anti-apoptotic effect and mechanism of farnesoid X receptor (FXR), and strategies of how to target FXR for inhibiting apoptosis implicated in liver fibrosis.

methodsSensitivity to apoptosis was compared between wild type and Fxr

findingsFXR deficiency sensitizes hepatocytes to death receptors (DRs)-engaged apoptosis. FXR overexpression, but not FXR ligands, inhibits apoptosis both in vitro and in vivo. Apoptotic stimuli lead to drastic reduction of FXR protein levels, a prerequisite for DRs-engaged apoptosis. Mechanistically, FXR interacts with caspase 8 (CASP8) in the cytoplasm, thus preventing the formation of death-inducing signaling complex (DISC) and activation of CASP8. Adenovirus-FXR transfection impedes liver fibrosis in CCl

interpretationFXR represents an intrinsic apoptosis inhibitor in hepatocytes and can be targeted via restoring its expression or strengthening FXR/CASP8 interaction for inhibiting hepatocytes apoptosis in liver fibrosis. FUND: National Natural Science Foundation of China.

Indexed as

ApoptosisAdenoviridaeAnimalsCarbon Tetrachloride PoisoningCaspase 8HepatocytesHumansLiver CirrhosisMaleMiceMice, KnockoutReceptor, Farnesoid X-ActivatedReceptors, Cytoplasmic and NuclearTransduction, GeneticCasp8 protein, mouseCaspase 8Receptor, Farnesoid X-ActivatedReceptors, Cytoplasmic and NuclearApoptosisCaspase 8FXRLiver fibrosisTransactivation independent

Identifiers

PMID30337250
PMCPMC6286639
OpenAlexW2896914840

What OpenQuestion holds

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LicenceCC BY-NC-ND
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.