Evidence map›Paper›PMID 42036682›Full record

ArticleStem cell research & therapy2026

iPSC-derived exosomes promote diabetic wound healing by attenuating inflammatory responses.

Li Long, Ju Qiao, Liang Wang, Yue Wang, Yi Xu, Hui Chen, Hongzhong Jin, Wei He, Xiaohong Han, Jianmin Zhang

Abstract read
In one paragraph

Article in Stem cell research & therapy, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. 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

10 authors.

Li LongDepartment of Immunology, CAMS Key laboratory T cell and Cancer Immunotherapy, Institute of Basic Medical Sciences, School of Basic Medicine, State Key Laboratory of Common Mechanism Research for Major Diseases, Chinese Academy of Medical Sciences, Peking Union Medical College, Beijing, 100005, China.
Ju QiaoDepartment of Dermatology, State Key Laboratory of Complex Severe and Rare Diseases, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, National Clinical Research Center for Dermatologic and Immunologic Diseases, Beijing, China.
Liang WangGuidon Pharmaceutics Ltd, Beijing, China.
Yue WangDepartment of Immunology, CAMS Key laboratory T cell and Cancer Immunotherapy, Institute of Basic Medical Sciences, School of Basic Medicine, State Key Laboratory of Common Mechanism Research for Major Diseases, Chinese Academy of Medical Sciences, Peking Union Medical College, Beijing, 100005, China.
Yi XuDepartment of Immunology, CAMS Key laboratory T cell and Cancer Immunotherapy, Institute of Basic Medical Sciences, School of Basic Medicine, State Key Laboratory of Common Mechanism Research for Major Diseases, Chinese Academy of Medical Sciences, Peking Union Medical College, Beijing, 100005, China.
Hui ChenDepartment of Immunology, CAMS Key laboratory T cell and Cancer Immunotherapy, Institute of Basic Medical Sciences, School of Basic Medicine, State Key Laboratory of Common Mechanism Research for Major Diseases, Chinese Academy of Medical Sciences, Peking Union Medical College, Beijing, 100005, China.
Hongzhong JinDepartment of Dermatology, State Key Laboratory of Complex Severe and Rare Diseases, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, National Clinical Research Center for Dermatologic and Immunologic Diseases, Beijing, China. jinhongzhong@263.net.
Wei HeDepartment of Immunology, CAMS Key laboratory T cell and Cancer Immunotherapy, Institute of Basic Medical Sciences, School of Basic Medicine, State Key Laboratory of Common Mechanism Research for Major Diseases, Chinese Academy of Medical Sciences, Peking Union Medical College, Beijing, 100005, China. heweingd@126.com.
Xiaohong HanClinical Pharmacology Research Center, Peking Union Medical College Hospital, State Key Laboratory of Complex Severe and Rare Diseases, NMPA Key Laboratory for Clinical Research and Evaluation of Drug, Beijing Key Laboratory of Clinical PK and PD Investigation for Innovative Drugs, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing, 100730, China. hanxiaohong@pumch.cn.
Jianmin ZhangDepartment of Immunology, CAMS Key laboratory T cell and Cancer Immunotherapy, Institute of Basic Medical Sciences, School of Basic Medicine, State Key Laboratory of Common Mechanism Research for Major Diseases, Chinese Academy of Medical Sciences, Peking Union Medical College, Beijing, 100005, China. jzhang42@163.com.

Funding

China Postdoctoral Science Foundation GZB20240072National High Level Hospital Clinical Research Funding 2022-PUMCH-B-092National High Level Hospital Clinical Research Funding 2022-PUMCH-C-059the CAMS Initiative for Innovative Medicine 2021-I2M-1-005the CAMS Initiative for Innovative Medicine 2021-I2M-1-035the CAMS Initiative for Innovative Medicine 2021-I2M-1-053the National Key Research and Development Program of China 2022YFC3602000the National Natural Science Foundation of China 82402139
6 · The paper itself

Abstract

backgroundOwing to impaired glucose metabolism, the high-glucose microenvironment in diabetic patients disrupts a series of biological reactions that hinder the wound healing process, resulting in a significant cost to the health care system and an urgent need for new and advanced therapies.

methodsIn this study, induced pluripotent stem cell-derived exosomes (iPSC-Exos) were isolated from iPSC culture supernatant via centrifugation and ultrafiltration. We evaluated the therapeutic effects of iPSC-Exos on diabetic wound healing through two clinically relevant animal models (spontaneous genetic diabetic mouse model and streptozotocin (STZ)-induced diabetic mouse model). iPSC-Exos were topically administered to full-thickness cutaneous wounds in diabetic mice. The therapeutic effects were systematically assessed by measuring wound closure rates, conducting comprehensive histopathological evaluations, and performing quantitative analysis of inflammatory mediators via ELISA.

resultsWe demonstrated that iPSC-Exos can significantly accelerate diabetic wound healing through two clinically relevant animal models (spontaneous genetic diabetic mouse model and STZ-induced diabetic mouse model) for the first time. The multifaceted therapeutic mechanisms include: (ⅰ) Direct activation of tissue regeneration (promotion of re-epithelialization, tissue remodeling and scar attenuation); (ⅱ) Modulation of the inflammatory microenvironment (promoting macrophage polarization toward anti-inflammatory M2 phenotype/suppressing inflammation).

conclusionsThis dual-animal model approach, which closely recapitulates key pathophysiological features of human diabetic wounds, offers superior clinical translatability compared to single-animal model studies. Our findings not only establish a robust scientific foundation for clinical development of iPSC-Exos therapy, but also present a transformative, cell-free treatment paradigm for chronic diabetic wounds that addresses critical unmet medical needs.

Indexed as

Diabetes Mellitus, ExperimentalExosomesInduced Pluripotent Stem CellsInflammationWound HealingAnimalsHumansMaleMiceMice, Inbred C57BLExosomesInduced pluripotent stem cellsInflammationRegenerationWound healing

Identifiers

PMID42036682
PMCPMC13255448

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Registered trials

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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 OpenQuestion graph.