Evidence map›Paper›PMID 32286145›Full record

ArticleCell cycle (Georgetown, Tex.)2020

YKL-40 mediates airway remodeling in asthma via activating FAK and MAPK signaling pathway.

Yu Sun, Zhaoquan Shi, Bing Liu, Xian'Gui Li, Ge Li, Feng Yang, Hao Tang

Open access · bronzeAbstract read
In one paragraph

Article in Cell cycle (Georgetown, Tex.), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed, 1 pooled it
1.9field-weighted citation impact, top 14% 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

19 citing papers in PubMed, 1 synthesis or guideline pooled it, 33 citations in OpenAlex.

  1. Pooled it
  2. Review
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  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Review
  10. Article
  11. Review
  12. Promising treatment biomarkers in asthma.Frontiers in drug safety and regulation · 2023
    Review
  13. Anti-asthmatic miR-224-5p inhibits the FHL1/MAPK pathway to repress airway smooth muscle cell proliferation in a murine model of asthma-like airway inflammation.Allergy, asthma, and clinical immunology : official journal of the Canadian Society of Allergy and Clinical Immunology · 2022
    Article
  14. Article
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  16. Article
  17. Network Pharmacology-Based Analysis of the Underlying Mechanism ofEvidence-based complementary and alternative medicine : eCAM · 2021
    Article
  18. 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

7 authors at 1 institution in 1 country.

Yu SunInsititute of Burn Surgery, Changhai Hospital, Second Military Medical University , Shanghai, China.
Zhaoquan ShiDepartment of Respiratory and Critical Care Medicine, Changzheng Hospital, Second Military Medical University , Shanghai, China.
Bing LiuDepartment of Respiratory Medicine, Shanghai Liqun Hospital , Shanghai, China.
Xian'Gui LiDepartment of Inorganic Chemistry, School of Pharmacy, Second Military Medical University , Shanghai, China.
Ge LiDepartment of Respiratory and Critical Care Medicine, Changzheng Hospital, Second Military Medical University , Shanghai, China.
Feng YangDepartment of Inorganic Chemistry, School of Pharmacy, Second Military Medical University , Shanghai, China.
Hao TangDepartment of Respiratory and Critical Care Medicine, Changzheng Hospital, Second Military Medical University , Shanghai, China.
Second Military Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

YKL-40 is a chitinase-like protein which was significantly elevated in asthma patients and related closely to asthma severity and airway remodeling. Airway remodeling in asthma involves complicated physical and pathological processes, including increased airway smooth muscle mass due to proliferation, migration of airway smooth muscle cells, epithelial-mesenchymal transition (EMT) and sub-epithelial fibrosis. However, the precise effect and underlying mechanism of YKL-40 in this pathological alteration remained unelucidated. In this study, we demonstrated that YKL-40 could promote asthma airway remodeling by increasing airway smooth muscle mass, inducing EMT and sub-epithelial fibrosis. Furthermore, we identified that FAK and MAPK signaling pathways are activated in the process. Inhibiting FAK or MAPK pathway could significantly ameliorate airway remodeling induced by excessive secretion of YKL-40

Indexed as

Airway RemodelingMAP Kinase Signaling SystemAnimalsAsthmaCell MovementCell ProliferationChitinase-3-Like Protein 1Cyclin D1Cyclin-Dependent KinasesDisease Models, AnimalEpithelial CellsEpithelial-Mesenchymal TransitionFibrosisFocal Adhesion Protein-Tyrosine KinasesHumansMice, Inbred C57BLChitinase-3-Like Protein 1Cyclin D1Cyclin-Dependent KinasesFocal Adhesion Protein-Tyrosine KinasesProtein Kinase InhibitorsProto-Oncogene Proteins c-aktsrc-Family Kinasesairway remodelingasthmaFAK and MAPKYKL-40

Identifiers

PMID32286145
PMCPMC7469639
OpenAlexW3015932121

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.