Evidence map›Paper›PMID 41516259›Full record

ReviewInternational journal of molecular sciences2025

Palmar Fascia Fibrosis in Dupuytren's Disease: A Narrative Review of Pathogenic Mechanisms and Molecular Insights.

Carmelo Pirri

Abstract readReview
In one paragraph

Review in International journal of molecular sciences, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing 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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

1 author.

Carmelo PirriDepartment of Neurosciences, Institute of Human Anatomy, University of Padua, 35121 Padova, Italy.ORCID 0000-0002-0119-6549

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Dupuytren's disease (DD) is a chronic fibroproliferative disorder of the palmar fascia, leading to disabling digital contractures and high recurrence after surgery. This narrative review highlights DD as a multifactorial condition in which genetic predisposition and cytogenetic instability converge with extracellular matrix remodeling, aberrant transforming growth factor β (TGF-β) and Wnt/β-catenin signaling, cytoskeletal stabilization and immune-inflammatory amplification. Epigenetic dysregulation further locks fibroblasts into a persistent myofibroblast state. Discrepancies between studies are largely explained by disease stage and experimental anti-inflammatory, antifibrotic and epigenetic strategies to achieve durable disease modification.

Indexed as

Dupuytren ContractureFasciaAnimalsEpigenesis, GeneticExtracellular MatrixFibrosisHumansMyofibroblastsTransforming Growth Factor betaWnt Signaling PathwayTransforming Growth Factor betaDupuytren’s diseaseepigeneticsextracellular matrixfibrosismyofibroblastpalmar fasciatransforming growth factor β

Identifiers

PMID41516259
PMCPMC12785835

What Socratic holds

Textmetadata
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 Socratic graph.