Evidence map›Paper›PMID 29497173›Full record

ArticleLaboratory investigation; a journal of technical methods and pathology2018

Pirfenidone reduces profibrotic responses in human dermal myofibroblasts, in vitro.

Caroline L Hall, Adrienne R Wells, Kai P Leung

Open access · bronzeAbstract read
PubMed Publisher
In one paragraph

Article in Laboratory investigation; a journal of technical methods and pathology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
4.7field-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

33 citing papers in PubMed, 46 citations in OpenAlex.

  1. Article
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  5. Article
  6. Biomolecules & biomedicine · 2024
    Article
  7. Article
  8. Modeling Molecular Mechanisms of Pirfenidone Interaction with Kinases.bioRxiv : the preprint server for biology · 2024
    Article
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  12. Review
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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

3 authors at 2 institutions in 1 country.

Caroline L HallDental and Craniofacial Trauma and Tissue Regeneration Directorate, United States Army Institute of Surgical Research, 3698 Chambers Pass, Building 3610, Joint Base San Antonio/Fort Sam Houston, TX, 78234, USA.
Adrienne R WellsDental and Craniofacial Trauma and Tissue Regeneration Directorate, United States Army Institute of Surgical Research, 3698 Chambers Pass, Building 3610, Joint Base San Antonio/Fort Sam Houston, TX, 78234, USA.
Kai P LeungDental and Craniofacial Trauma and Tissue Regeneration Directorate, United States Army Institute of Surgical Research, 3698 Chambers Pass, Building 3610, Joint Base San Antonio/Fort Sam Houston, TX, 78234, USA. kai.p.leung.civ@mail.mil.
United States Army Institute of Surgical Research · USJoint Base San Antonio · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pirfenidone (PFD) is a synthetic small molecule inhibitor with demonstrated anti-inflammatory and antifibrotic properties in vitro and in vivo. The exact mechanism(s) of PFD action remain unclear, due in part to the broad effects of this drug on the complex processes involved in inflammation and fibrosis. While PFD is FDA-approved for the treatment of idiopathic pulmonary fibrosis, the efficacy of this compound for the treatment of dermal fibrosis has not yet been fully characterized. Dermal fibrosis is the pathological formation of excess fibrous connective tissue of the skin, usually the result of traumatic cutaneous injury. Fibroproliferative scarring, caused by delayed wound healing and prolonged inflammation, remains a major clinical concern with considerable morbidity. Despite efforts to identify a therapeutic that targets the fibrotic pathways involved in wound healing to mitigate scar formation, no satisfactory dermal antifibrotic has yet been identified. We aim to better elucidate the antifibrotic mechanism(s) of PFD activity using an in vitro model of dermal fibrosis. Briefly, cultured human dermal fibroblasts were stimulated with TGF-β1 to induce differentiation into profibrotic myofibroblast cells. A dose-dependent reduction in cellular proliferation and migration was observed in TGF-β1-stimulated cells when treated with PFD. We observed a clear inhibition in the development of essential myofibroblast mechanoregulatory machinery, including contractile F-actin stress fibers containing α-SMA and large super-mature focal adhesions. PFD treatment significantly reduced protein levels of major ECM components type I and type III collagen. PFD targeted the p38 MAPK signaling pathway and mitigated profibrotic gene expression profiles. This in vitro data promotes PFD as a potential therapeutic agent for the treatment of dermal fibrosis.

Indexed as

ActinsCell DifferentiationCell ProliferationCells, CulturedCollagenFibrosisHumansMAP Kinase Signaling SystemMyofibroblastsp38 Mitogen-Activated Protein KinasesPyridonesSkinTransforming Growth Factor beta1ACTA2 protein, humanActinsCollagenp38 Mitogen-Activated Protein KinasespirfenidonePyridonesTransforming Growth Factor beta1

Identifiers

PMID29497173
OpenAlexW2789635721

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.