Evidence map›Paper›PMID 33398723›Full record

ArticleJournal of cell communication and signaling2021

Verteporfin inhibits the persistent fibrotic phenotype of lesional scleroderma dermal fibroblasts.

Xu Shi-Wen, Michael Racanelli, Aaisham Ali, Amara Simon, Katherine Quesnel, Richard J Stratton, Andrew Leask

Open access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of cell communication and signaling, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
5.0field-weighted citation impact, top 4% 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

24 citing papers in PubMed, 40 citations in OpenAlex.

  1. Article
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  6. Research progress on Hippo signaling pathway effector molecules in rheumatic immune system diseases.Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2024
    Review
  7. Review
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Studying the Geroprotective Properties of YAP/TAZ Signaling Inhibitors onInternational journal of molecular sciences · 2023
    Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Review
  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

7 authors at 3 institutions in 2 countries.

Xu Shi-WenUCL Division of Medicine, Centre for Rheumatology, University College London, Royal Free Campus, Rowland Hill St, London, NW3 2PF, UK.
Michael RacanelliDepartment of Physiology and Pharmacology, University of Western Ontario, London, ON, N6A 5C1, Canada.
Aaisham AliDepartment of Physiology and Pharmacology, University of Western Ontario, London, ON, N6A 5C1, Canada.
Amara SimonDepartment of Physiology and Pharmacology, University of Western Ontario, London, ON, N6A 5C1, Canada.
Katherine QuesnelSchool of Dentistry, University of Western Ontario, London, ON, N6A 5C1, Canada.
Richard J StrattonUCL Division of Medicine, Centre for Rheumatology, University College London, Royal Free Campus, Rowland Hill St, London, NW3 2PF, UK.
Andrew LeaskCollege of Dentistry, University of Saskatchewan, 105 Wiggins Rd, Saskatoon, SK, S7N 5E4, Canada. anl312@usask.ca.ORCID http://orcid.org/0000-0003-2832-283X
Western University · CAThe Royal Free Hospital · GBUniversity of Saskatchewan · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Fibrosis is perpetuated by an autocrine, pro-adhesive signaling loop maintained by the synthetic and contractile abilities of myofibroblasts and the stiff, highly-crosslinked extracellular matrix. Transcriptional complexes that are exquisitely responsive to mechanotransduction include the co-activator YAP1, which regulates the expression of members of the CCN family of matricellular proteins such as CCN2 and CCN1. Although selective YAP1 inhibitors exist, the effect of these inhibitors on profibrotic gene expression in fibroblasts is largely unknown, and is the subject of our current study. Herein, we use genome-wide expression profiling, real-time polymerase chain reaction and Western blot analyses, cell migration and collagen gel contraction assays to assess the ability of a selective YAP inhibitor verteporfin (VP) to block fibrogenic activities in dermal fibroblasts from healthy individual human controls and those from isolated from fibrotic lesions of patients with diffuse cutaneous systemic sclerosis (dcSSc). In control fibroblasts, VP selectively reduced expression of fibrogenic genes and also blocked the ability of TGFbeta to induce actin stress fibers in dermal fibroblasts. VP also reduced the persistent profibrotic phenotype of dermal fibroblasts cultured from fibrotic lesions of patients with dcSSc. Our results are consistent with the notion that, in the future, YAP1 inhibitors may represent a novel, valuable method of treating fibrosis as seen in dcSSc.

Indexed as

CCN2Connective tissue growth factorCTGFFibrosisMechanotransductionMyofibroblasrSclerodermaVerteporfinYAP1

Identifiers

PMID33398723
PMCPMC7905010
OpenAlexW3118889770

What Socratic 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 Socratic graph.