Evidence map›Paper›PMID 37958797›Full record

ArticleInternational journal of molecular sciences2023

NLRP3 Inflammasome Activates Endothelial-to-Mesenchymal Transition via Focal Adhesion Kinase Pathway in Bleomycin-Induced Pulmonary Fibrosis.

Wei-Chih Chen, Wen-Kuang Yu, Vincent Yi-Fong Su, Han-Shui Hsu, Kuang-Yao Yang

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
4.1field-weighted citation impact, top 5% 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

12 citing papers in PubMed, 16 citations in OpenAlex.

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  12. [Normal mouse serum alleviates radiation pneumonitis in mice by inhibiting the focal adhesion signaling pathway].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2024
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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

5 authors at 1 institution in 1 country.

Wei-Chih ChenInstitute of Emergency and Critical Care Medicine, College of Medicine, National Yang Ming Chiao Tung University, Taipei 112, Taiwan.ORCID 0000-0003-4172-5529
Wen-Kuang YuSchool of Medicine, College of Medicine, National Yang Ming Chiao Tung University, Taipei 112, Taiwan.
Vincent Yi-Fong SuSchool of Medicine, College of Medicine, National Yang Ming Chiao Tung University, Taipei 112, Taiwan.
Han-Shui HsuInstitute of Emergency and Critical Care Medicine, College of Medicine, National Yang Ming Chiao Tung University, Taipei 112, Taiwan.
Kuang-Yao YangInstitute of Emergency and Critical Care Medicine, College of Medicine, National Yang Ming Chiao Tung University, Taipei 112, Taiwan.ORCID 0000-0002-2803-980X
National Yang Ming Chiao Tung University · TW

Funding

Ministry of Education 111W31101Ministry of Education 112W31101National Science and Technology Council MOST 105-2314-B-010-041-MY3National Science and Technology Council MOST 109-2314-B-010-051-MY3National Science and Technology Council NSTC 112-2314-B-075-050National Science and Technology Council NSTC 112-2314-B-A49-040National Yang Ming Chiao Tung University 108-V-A-005Taipei Veterans General Hospital V108C-057Taipei Veterans General Hospital V109C-033Taipei Veterans General Hospital V111B-024Taipei Veterans General Hospital V111C-050Taipei Veterans General Hospital V112B-031Taipei Veterans General Hospital V112C-068
6 · The paper itself

Abstract

Idiopathic pulmonary fibrosis has poor clinical outcomes despite antifibrotic treatment. The nucleotide-binding domain leucine-rich repeat-containing receptor, pyrin domain-containing-3 (NLRP3) inflammasome and endothelial-to-mesenchymal transition (EndoMT) were shown to be involved in the pathogenesis of pulmonary fibrosis. However, the detailed mechanism is unknown. Our study aimed to investigate the role of the NLRP3 inflammasome in the regulation of EndoMT in pulmonary fibrosis. The inhibition of the NLRP3 inflammasome via a caspase-1 inhibitor, Ac-YVAD-cmk (YVAD), was intraperitoneally administered to male C57BL/6 mice (8-12 weeks old) one hour before bleomycin intratracheal injection (1.5 U/kg). Immunohistochemical staining, Masson's trichrome staining, enzyme-linked immunosorbent assay, immunofluorescence, and Western blotting were used to assess the activity of the NLRP3 inflammasome and EndoMT in lung samples from mice. Human pulmonary microvascular endothelial cells (HPMECs) were used as a model of EndoMT in vitro with YVAD and bleomycin stimulation. We observed the activation of the NLRP3 inflammasome and EndoMT (decreased vascular endothelial cadherin with increased alpha-smooth muscle actin and vimentin) in the lung samples after bleomycin. However, inhibition of the NLRP3 inflammasome significantly reduces EndoMT via inhibiting focal adhesion kinase (FAK). In vitro studies also confirmed these findings. In conclusion, NLRP3 inflammasome inhibition could reduce lung inflammation and fibrosis via the regulation of EndoMT by the FAK pathway.

Indexed as

Pulmonary FibrosisAnimalsBleomycinEndothelial CellsFibrosisFocal Adhesion Protein-Tyrosine KinasesHumansInflammasomesMaleMiceMice, Inbred C57BLNLR Family, Pyrin Domain-Containing 3 ProteinBleomycinFocal Adhesion Protein-Tyrosine KinasesInflammasomesNLR Family, Pyrin Domain-Containing 3 Proteincaspase-1 inhibitorendothelial-to-mesenchymal transitionfocal adhesion kinasenucleotide-binding domain leucine-rich repeat-containing receptorpulmonary fibrosispyrin domain-containing-3 (NLRP3) inflammasome

Identifiers

PMID37958797
PMCPMC10648980
OpenAlexW4388042205

What OpenQuestion holds

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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.