Evidence map›Paper›PMID 32793588›Full record

ArticleFrontiers in cell and developmental biology2020

Disruption of FGF Signaling Ameliorates Inflammatory Response in Hepatic Stellate Cells.

Cong Wang, Yuelong Li, Hao Li, Yali Zhang, Zhangguo Ying, Xuye Wang, Tingting Zhang, Wenshu Zhang, Zhichao Fan, Xiaokun Li and 2 more

Open access · goldAbstract read
In one paragraph

Article in Frontiers in cell and developmental biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
2.2field-weighted citation impact, top 12% 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

26 citing papers in PubMed, 37 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. Article
  20. 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

12 authors at 1 institution in 1 country.

Cong WangSchool of Pharmaceutical Sciences, Wenzhou Medical University, Wenzhou, China.
Yuelong LiSchool of Pharmaceutical Sciences, Wenzhou Medical University, Wenzhou, China.
Hao LiSchool of Pharmaceutical Sciences, Wenzhou Medical University, Wenzhou, China.
Yali ZhangSchool of Pharmaceutical Sciences, Wenzhou Medical University, Wenzhou, China.
Zhangguo YingSchool of Pharmaceutical Sciences, Wenzhou Medical University, Wenzhou, China.
Xuye WangSchool of Pharmaceutical Sciences, Wenzhou Medical University, Wenzhou, China.
Tingting ZhangSchool of Pharmaceutical Sciences, Wenzhou Medical University, Wenzhou, China.
Wenshu ZhangSchool of Pharmaceutical Sciences, Wenzhou Medical University, Wenzhou, China.
Zhichao FanSchool of Pharmaceutical Sciences, Wenzhou Medical University, Wenzhou, China.
Xiaokun LiSchool of Pharmaceutical Sciences, Wenzhou Medical University, Wenzhou, China.
Jisheng MaSchool of Pharmaceutical Sciences, Wenzhou Medical University, Wenzhou, China.
Xuebo PanSchool of Pharmaceutical Sciences, Wenzhou Medical University, Wenzhou, China.
Wenzhou Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

It is a well-documented event that fibroblast growth factors (FGFs) regulate liver development and homeostasis in autocrine, paracrine, and endocrine manners via binding and activating FGF receptors (FGFRs) tyrosine kinase in hepatocytes. Recent research reveals that hepatic stellate cells (HSCs) play a fundamental role in liver immunology. However, how FGF signaling in HSCs regulates liver inflammation remains unclear. Here, we report that FGF promoted NF-κB signaling, an inflammatory pathway, in human HSCs, which was associated with FGFR1 expression. Both FGF and NF-κB signaling in HSCs were compromised by FGFR1 tyrosine kinase inhibitor. After stimulating HSCs with proinflammatory cytokines, expression of multiple FGF ligands was significantly increased. However, disruption of FGF signaling with FGFR inhibitors prominently reduced the apoptosis, inflammatory response, NF-κB nuclear translocation, and expression of matrix metalloproteinase-9 (MMP-9) induced by TNFα in HSCs. Interestingly, FGF21 significantly alleviated the inflammation responses in the concanavalin A (Con A)-induced acutely injured liver. Unlike canonic FGFs that elicit signals through activating the FGFR-heparan sulfate complex, FGF21 activates the FGFR-KLB complex and elicits a different set of signals. Therefore, the finding here indicates the urgency of developing pathway-specific inhibitors that only suppress canonical FGF, but not non-canonical FGF21, signaling for alleviating inflammation in the liver, which is presented in all stages of diseased liver.

Indexed as

FGFRhepatic stellate cellinflammationMMP9NF-κB

Identifiers

PMID32793588
PMCPMC7387415
OpenAlexW3044467369

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.