Evidence map›Paper›PMID 34439762›Full record

ReviewBiomolecules2021

Myofibroblasts: Function, Formation, and Scope of Molecular Therapies for Skin Fibrosis.

Yifan Tai, Emma L Woods, Jordanna Dally, Deling Kong, Robert Steadman, Ryan Moseley, Adam C Midgley

Abstract readReview
In one paragraph

Review in Biomolecules, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 142 papers.

0numbers the graph read from it
0cells of the map it votes in
142citing papers in PubMed
–field-weighted citation impact
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

142 citing papers in PubMed.

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  15. Molecular mechanisms of ovarian fibrosis.Molecular human reproduction · 2026
    Review
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82 more citing papers are in PubMed but not listed here.

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.

Yifan TaiKey Laboratory of Bioactive Materials for the Ministry of Education, College of Life Sciences, Nankai University, Tianjin 300071, China.
Emma L WoodsWelsh Kidney Research Unit, Division of Infection and Immunity, Cardiff Institute of Tissue Engineering and Repair (CITER), School of Medicine, Cardiff University, Heath Park, Cardiff CF14 4XN, UK.
Jordanna DallyWelsh Kidney Research Unit, Division of Infection and Immunity, Cardiff Institute of Tissue Engineering and Repair (CITER), School of Medicine, Cardiff University, Heath Park, Cardiff CF14 4XN, UK.ORCID 0000-0002-2221-2683
Deling KongKey Laboratory of Bioactive Materials for the Ministry of Education, College of Life Sciences, Nankai University, Tianjin 300071, China.
Robert SteadmanWelsh Kidney Research Unit, Division of Infection and Immunity, Cardiff Institute of Tissue Engineering and Repair (CITER), School of Medicine, Cardiff University, Heath Park, Cardiff CF14 4XN, UK.
Ryan MoseleyRegenerative Biology Group, Oral and Biomedical Sciences, Cardiff Institute of Tissue Engineering and Repair (CITER), School of Dentistry, Cardiff University, Heath Park, Cardiff CF14 4XY, UK.ORCID 0000-0002-2812-6735
Adam C MidgleyKey Laboratory of Bioactive Materials for the Ministry of Education, College of Life Sciences, Nankai University, Tianjin 300071, China.ORCID 0000-0002-7622-0275

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Myofibroblasts are contractile, α-smooth muscle actin-positive cells with multiple roles in pathophysiological processes. Myofibroblasts mediate wound contractions, but their persistent presence in tissues is central to driving fibrosis, making them attractive cell targets for the development of therapeutic treatments. However, due to shared cellular markers with several other phenotypes, the specific targeting of myofibroblasts has long presented a scientific and clinical challenge. In recent years, myofibroblasts have drawn much attention among scientific research communities from multiple disciplines and specialisations. As further research uncovers the characterisations of myofibroblast formation, function, and regulation, the realisation of novel interventional routes for myofibroblasts within pathologies has emerged. The research community is approaching the means to finally target these cells, to prevent fibrosis, accelerate scarless wound healing, and attenuate associated disease-processes in clinical settings. This comprehensive review article describes the myofibroblast cell phenotype, their origins, and their diverse physiological and pathological functionality. Special attention has been given to mechanisms and molecular pathways governing myofibroblast differentiation, and updates in molecular interventions.

Indexed as

ActinsAnimalsbeta CateninCell DifferentiationCells, CulturedCicatrixErbB ReceptorsFibrosisHumansHyaluronan ReceptorsHyaluronic AcidLigandsMiceMyofibroblastsPhenotypeSignal TransductionActinsbeta CateninCD44 protein, humanErbB ReceptorsHyaluronan ReceptorsHyaluronic AcidLigandsSmad ProteinsTgfb1 protein, mouseTransforming Growth Factor beta1Wnt Proteinsanti-scarring therapyfibrosismyofibroblasttransforming growth factor-β1wound healing

Identifiers

PMID34439762
PMCPMC8391320

What OpenQuestion holds

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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.