Evidence map›Paper›PMID 40369633›Full record

ArticleStem cell research & therapy2025

Human umbilical cord mesenchymal stem cell therapy for atopic dermatitis through inhibition of neutrophil chemotaxis.

Jinjin Shao, Zhiqi Xie, Zhichao Ye, Guoyu Chen, Yiru Wang, Lili Zhang, Fang Liu, Siming Zhang, Xiaobo Lin, Jiahong Wang and 7 more

Abstract read
In one paragraph

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.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed, 1 pooled it
–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

4 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Article
  3. Review
  4. Review
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

17 authors.

Jinjin Shao *Key Laboratory of Drug Safety Evaluation and Research of Zhejiang Province, Center of Safety Evaluation and Research, Hangzhou Medical College, Hangzhou, 310053, China.
Zhiqi Xie *Wuyi First People's Hospital, Affiliated Hospital, School of Medicine, Hangzhou City University, Hangzhou, 310015, China.
Zhichao YeKey Laboratory of Drug Safety Evaluation and Research of Zhejiang Province, Center of Safety Evaluation and Research, Hangzhou Medical College, Hangzhou, 310053, China.
Guoyu ChenKey Laboratory of Drug Safety Evaluation and Research of Zhejiang Province, Center of Safety Evaluation and Research, Hangzhou Medical College, Hangzhou, 310053, China.
Yiru WangFaculty of Chinese Medicine, Macau University of Science and Technology, Macao, 999078, China.
Lili ZhangKey Laboratory of Drug Safety Evaluation and Research of Zhejiang Province, Center of Safety Evaluation and Research, Hangzhou Medical College, Hangzhou, 310053, China.
Fang LiuKey Laboratory of Drug Safety Evaluation and Research of Zhejiang Province, Center of Safety Evaluation and Research, Hangzhou Medical College, Hangzhou, 310053, China.
Siming ZhangKey Laboratory of Drug Safety Evaluation and Research of Zhejiang Province, Center of Safety Evaluation and Research, Hangzhou Medical College, Hangzhou, 310053, China.
Xiaobo LinKey Laboratory of Drug Safety Evaluation and Research of Zhejiang Province, Center of Safety Evaluation and Research, Hangzhou Medical College, Hangzhou, 310053, China.
Jiahong WangKey Laboratory of Drug Safety Evaluation and Research of Zhejiang Province, Center of Safety Evaluation and Research, Hangzhou Medical College, Hangzhou, 310053, China.
Ying ChenKey Laboratory of Drug Safety Evaluation and Research of Zhejiang Province, Center of Safety Evaluation and Research, Hangzhou Medical College, Hangzhou, 310053, China.
Yunxiang ChenKey Laboratory of Drug Safety Evaluation and Research of Zhejiang Province, Center of Safety Evaluation and Research, Hangzhou Medical College, Hangzhou, 310053, China.
Xin PanZhejiang Key Laboratory of Cell-Based Drug and Applied Technology Development, S-Evans Biosciences Co., Ltd., Hangzhou, China.
Feifei WuZhejiang Key Laboratory of Cell-Based Drug and Applied Technology Development, S-Evans Biosciences Co., Ltd., Hangzhou, China.
Ruolang PanZhejiang Key Laboratory of Cell-Based Drug and Applied Technology Development, S-Evans Biosciences Co., Ltd., Hangzhou, China. panrl@zju.edu.cn.
Jinfeng LiangZhejiang Center for Drugs and Cosmetics Evaluation, Zhejiang Province Food and Drug Administration, Hangzhou, 310012, China. liangwind@sohu.com.
Lijiang ZhangKey Laboratory of Drug Safety Evaluation and Research of Zhejiang Province, Center of Safety Evaluation and Research, Hangzhou Medical College, Hangzhou, 310053, China. zhanglj127@163.com.ORCID http://orcid.org/0000-0002-7902-0893

Funding

Key Research and Development Program of Zhejiang Province 2021C03077National Natural Science Foundation of China 82404122
6 · The paper itself

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.

Indexed as

ChemotaxisDermatitis, AtopicMesenchymal Stem CellsMesenchymal Stem Cell TransplantationNeutrophilsUmbilical CordAnimalsCulture Media, ConditionedDisease Models, AnimalExosomesFemaleHumansMiceSTAT3 Transcription FactorCulture Media, ConditionedSTAT3 Transcription FactorAtopic dermatitisHuman umbilical cord mesenchymal stem cellsJAK-STAT signaling pathwayKeratinocytesNeutrophil chemotaxis

Identifiers

PMID40369633
PMCPMC12079922

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
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.