Level D· Scientific groundwork from lab and animal studiesAnimal StudyPubMedOpen access

The stromal vascular fraction mitigates bleomycin-induced skin fibrosis in mice by modulating vascular lesions and secreting antifibrotic factors at different stages of disease.

Wang Z., Shi M., Liu Z., Chen Y., Shi X., Wang J.

Animal Study on Autoimmune Research, published in Stem Cell Res Ther (2025) — summary generated from the PubMed abstract.

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Level D· Scientific groundwork from lab and animal studiesEvidence level of this study

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

  • Level A · Stronger Clinical Evidence
  • Level B · Emerging clinical evidence with positive signals
  • Level C · Early human research exploring benefits
  • Level D · Scientific groundwork from lab and animal studies
  • Emerging · Emerging topic under active research
Read the A–D evidence level guide

This page is generated from the PubMed record. The Thai description is an automated summary of bibliographic fields and the abstract, not a full translation, and is not medical advice.

Study type
Animal Study
Journal
Stem Cell Res Ther (2025)
Country
England
Reported sample size
—
Source database
PubMed
PMID
40597400
PMCID
PMC12210721
DOI
10.1186/s13287-025-04470-8
Citations
1

Abstract (original English)

Background Systemic sclerosis (SSc) is a chronic autoimmune disease characterized by fibrosis of the skin and internal organs, leading to significant morbidity and reduced quality of life. Despite ongoing research, the underlying pathogenesis of SSc remains unclear, and treatment options are limited. Stromal vascular fraction (SVF), a naturally occurring cell population that includes mesenchymal stem cells (MSCs), has emerged as a potential therapeutic agent for various fibrotic diseases. This study aimed to investigate the therapeutic effects and underlying mechanisms of SVF in a bleomycin-induced mouse model of skin fibrosis. Methods SVF was isolated from the inguinal adipose tissue of C57BL/6 mice and administered subcutaneously or intradermally at different disease stages to assess its impact on skin fibrosis. Histological analyses were performed to evaluate dermal thickness and collagen deposition. In vivo imaging and immunofluorescence were used to track the retention of SVF within fibrotic tissue over time, particularly in the subcutaneous layer. Flow cytometry and immunofluorescence were employed to examine cutaneous vascular pathology and the secretion of antifibrotic factors, such as hepatocyte growth factor (HGF) and basic fibroblast growth factor (FGF-2). Finally, we investigated the contribution of major SVF subsets to cutaneous fibrosis and the mechanisms by which

What this study does not prove

  • • This study does not prove SVF is an approved treatment or a replacement for standard care.
  • • This is preclinical work; animal or laboratory results cannot be applied to humans.

Evidence level

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

How we grade evidence
AnimalsBleomycinFibrosisMiceMice, Inbred C57BLSkinScleroderma, SystemicMesenchymal Stem CellsHepatocyte Growth FactorDisease Models, Animal

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