Evidence map›Paper›PMID 40232216›Full record

ArticleThe Journal of hand surgery2026

Transforming Myofibroblasts Into Lipid-Filled Cells to Treat Dupuytren Disease.

Mary E Ziegler, Melinda Lem, Jacklyn Melkonian, Tania Nasrollahi, Helia Rahimian, Abtin Shams, Nikhil Prabhakar, Seyedeh Saina Saifzadeh, Amalvin Fritz, Amber Leis and 1 more

Abstract read
In one paragraph

Article in The Journal of hand surgery, 2026. 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

11 authors.

Mary E ZieglerCenter for Tissue Engineering, Department of Plastic Surgery, University of California, Orange, CA.
Melinda LemCenter for Tissue Engineering, Department of Plastic Surgery, University of California, Orange, CA.
Jacklyn MelkonianCenter for Tissue Engineering, Department of Plastic Surgery, University of California, Orange, CA.
Tania NasrollahiCenter for Tissue Engineering, Department of Plastic Surgery, University of California, Orange, CA.
Helia RahimianCenter for Tissue Engineering, Department of Plastic Surgery, University of California, Orange, CA.
Abtin ShamsCenter for Tissue Engineering, Department of Plastic Surgery, University of California, Orange, CA.
Nikhil PrabhakarCenter for Tissue Engineering, Department of Plastic Surgery, University of California, Orange, CA.
Seyedeh Saina SaifzadehCenter for Tissue Engineering, Department of Plastic Surgery, University of California, Orange, CA.
Amalvin FritzCenter for Tissue Engineering, Department of Plastic Surgery, University of California, Orange, CA.
Amber LeisDepartment of Plastic Surgery, University of California, Orange, CA.
Alan WidgerowCenter for Tissue Engineering, Department of Plastic Surgery, University of California, Orange, CA. Electronic address: awidgero@hs.uci.edu.

Funding

Institute for Clinical and Translational ScienceUM1TR004927 · NCATS · UNIVERSITY OF CALIFORNIA-IRVINE · PI DAN M COOPER, Eric J. Vilain · 2024 to 2026
$12.2M
NCATS NIH HHS UM1 TR004927
6 · The paper itself

Abstract

purposeTransforming myofibroblasts (MFs) into adipocyte-like cells may be a viable option for treating Dupuytren disease. Human Dupuytren MFs (DMFs) and adipose-derived stem cells (ASCs) cocultured in the presence of platelet-rich plasma (PRP) reprogrammed into lipid-laden cells. This treatment also reduced fibrosis markers in vivo. We aimed to determine whether this treatment transformed DMFs into adipocyte-like cells in vivo and characterize the PRP factors contributing to this transformation.

methodsDupuytren MFs and normal human dermal fibroblasts were transplanted into the forepaws of rats (Rowett Nude [rnu/rnu]). Two months later, the paws were treated with saline, ASCs + PRP, or Clostridium histolyticum (clinical comparison) once a week for three treatments. The paw tissue was harvested 1 week after each treatment and subjected to Masson trichrome staining, collagen I and III, α-smooth muscle actin (SMA), and perilipin detection by immunohistochemistry. Dupuytren MFs were cocultured with ASCs and PRP or insulin-like growth factor I (IGF-I) or IGF-I-depleted PRP. In addition, the IGF-I receptor was inhibited. Oil Red O or boron-dipyrromethene detected lipid-laden cells.

resultsRodent paws implanted with DMFs showed enhanced α-SMA expression, imbalanced collagen III:I ratio, and reduced adipocytes compared with normal human dermal fibroblasts. After treatment with ASCs + PRP, DMF paws demonstrated reduced α-SMA, a balanced collagen III:I ratio, and a replenishment of adipocytes. Dupuytren MFs treated with ASCs + IGF-I transformed into adipocyte-like cells in vitro, which was validated by IGF-I-depletion and IGF-I receptor inhibition.

conclusionsAdipose-derived stem cells + PRP reduce fibrosis markers and induce adipocyte renewal in vivo. As a PRP component, IGF-I works with ASCs to transform DMFs into adipocyte-like cells in vitro. CLINICAL RELEVANCE: Identifying an active factor in PRP that synergizes with ASCs to transform DMFs into adipocyte-like cells may contribute to finding a novel therapeutic for Dupuytren disease. Such a treatment may allow for less-extensive surgical intervention coupled with therapeutic injection to reduce the recurrence of Dupuytren disease.

Indexed as

AdipocytesDupuytren ContractureMyofibroblastsAdipose TissueAnimalsCoculture TechniquesDisease Models, AnimalFibroblastsHumansPlatelet-Rich PlasmaRatsRats, NudeAdipose-derived stem cellsDupuytren diseasefibrosislipodystrophymyofibroblasts

Identifiers

PMID40232216
PMCPMC13089957

What Socratic holds

Textmetadata
LicenceTDM
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.