ArticleStem cell research & therapy2025
Human umbilical cord mesenchymal stem cell therapy for atopic dermatitis through inhibition of neutrophil chemotaxis.
Article in Stem cell research & therapy, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers, 1 of them a synthesis that pooled it.
What it found
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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.
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.
Who cites it
4 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Review: progression and heterogeneity of multiple sources of mesenchymal stromal cells for the treatment of rheumatoid arthritis.Stem cell research & therapy · 2025Pooled it
- The Secretome Derived From Human Umbilical Cord Mesenchymal Stem Cells Improves Skin Photoaging by Enhancing Mitophagy to Inhibit the cGAS-STING Pathway.Aging cell · 2026Article
- Targeting the JAK/STAT pathway in atopic dermatitis.Frontiers in immunology · 2026Review
- Extracellular vesicles in atopic dermatitis: unraveling pathogenic mediators and engineering therapeutic vectors.Frontiers in immunology · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
17 authors.
Funding
Abstract
backgroundAtopic dermatitis (AD) management is significantly challenging due to the high prevalence, chronicity, and recurrent nature of the disease, and limited options for its treatment. Human umbilical cord mesenchymal stem cells (hUC-MSCs) exhibit potential effects against AD; however, the mechanisms underlying these effects remain largely unexplored.
methodsAD mouse models were established using 1-chloro-2,4-dinitrobenzene (DNCB) and ovalbumin (OVA). The therapeutic effects of subcutaneously administered hUC-MSCs and their conditioned medium (hUC-MSC-CM) were evaluated through histopathology, western blotting, PCR, ELISA, and flow cytometry. Mechanistic studies included RNA sequencing, cytokine arrays, and exosome characterization.
resultsBoth hUC-MSCs and hUC-MSC-CM significantly alleviated AD-like symptoms, including erythema, epidermal thickening, and inflammatory cell infiltration in DNCB- and OVA-induced models. There was a decrease in serum IgE levels and histological analyses confirmed attenuated skin damage in these models. Moreover, neither hUC-MSCs nor hUC-MSC-CM induced weight loss. Mechanistically, hUC-MSC-CM suppressed neutrophil migration in the skin and inhibited keratinocyte-derived chemokine (e.g., CCL5 and CXCL11) secretion. Additionally, hUC-MSC-derived exosomes reduced chemokine production in keratinocytes, mediated by the STAT3 signaling pathway.
conclusionsThis study demonstrated that hUC-MSCs and hUC-MSC-CM ameliorate AD-like symptoms, possibly through exosome-dependent suppression of the STAT3 signaling pathway and chemokine expression. Furthermore, hUC-MSC-CM serves as a cell-free alternative to whole-cell therapy, with comparable efficacy, offering novel mechanistic insights and a potential translational strategy for AD treatment.
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What Socratic holds
Registered trials
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.