Evidence map›Paper›PMID 41146891›Full record

ArticleBurns & trauma2025

Fibroblast exosomes promote wound healing and improve the quality of healed skin via miR-29a-3p-mediated KEAP1/Nrf2 pathway activation.

Lingfeng Yan, Dejiang Fan, Jiacai Yang, Jue Wang, Xiaohong Hu, Xiaorong Zhang, Yong Huang, Hong Wang, Wenjing Yin, Xin Cai and 4 more

Abstract read
In one paragraph

Article in Burns & trauma, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing 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

8 citing papers in PubMed.

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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

14 authors.

Lingfeng YanInstitute of Burn Research, State Key Laboratory of Trauma and Chemical Poisoning, the First Affiliated Hospital of Army Medical University (the Third Military Medical University), 30 Gaotanyan Main Street, Shapingba District, Chongqing 400038, China.
Dejiang FanInstitute of Burn Research, State Key Laboratory of Trauma and Chemical Poisoning, the First Affiliated Hospital of Army Medical University (the Third Military Medical University), 30 Gaotanyan Main Street, Shapingba District, Chongqing 400038, China.
Jiacai YangInstitute of Burn Research, State Key Laboratory of Trauma and Chemical Poisoning, the First Affiliated Hospital of Army Medical University (the Third Military Medical University), 30 Gaotanyan Main Street, Shapingba District, Chongqing 400038, China.
Jue WangInstitute of Burn Research, State Key Laboratory of Trauma and Chemical Poisoning, the First Affiliated Hospital of Army Medical University (the Third Military Medical University), 30 Gaotanyan Main Street, Shapingba District, Chongqing 400038, China.
Xiaohong HuInstitute of Burn Research, State Key Laboratory of Trauma and Chemical Poisoning, the First Affiliated Hospital of Army Medical University (the Third Military Medical University), 30 Gaotanyan Main Street, Shapingba District, Chongqing 400038, China.
Xiaorong ZhangInstitute of Burn Research, State Key Laboratory of Trauma and Chemical Poisoning, the First Affiliated Hospital of Army Medical University (the Third Military Medical University), 30 Gaotanyan Main Street, Shapingba District, Chongqing 400038, China.
Yong HuangInstitute of Burn Research, State Key Laboratory of Trauma and Chemical Poisoning, the First Affiliated Hospital of Army Medical University (the Third Military Medical University), 30 Gaotanyan Main Street, Shapingba District, Chongqing 400038, China.
Hong WangInstitute of Burn Research, State Key Laboratory of Trauma and Chemical Poisoning, the First Affiliated Hospital of Army Medical University (the Third Military Medical University), 30 Gaotanyan Main Street, Shapingba District, Chongqing 400038, China.
Wenjing YinInstitute of Burn Research, State Key Laboratory of Trauma and Chemical Poisoning, the First Affiliated Hospital of Army Medical University (the Third Military Medical University), 30 Gaotanyan Main Street, Shapingba District, Chongqing 400038, China.
Xin CaiInstitute of Burn Research, State Key Laboratory of Trauma and Chemical Poisoning, the First Affiliated Hospital of Army Medical University (the Third Military Medical University), 30 Gaotanyan Main Street, Shapingba District, Chongqing 400038, China.
Ruoyu ShangInstitute of Burn Research, State Key Laboratory of Trauma and Chemical Poisoning, the First Affiliated Hospital of Army Medical University (the Third Military Medical University), 30 Gaotanyan Main Street, Shapingba District, Chongqing 400038, China.
Canhua HuangState Key Laboratory of Biotherapy and Cancer Center, West China Hospital, and West China School of Basic Medical Sciences & Forensic Medicine, Sichuan University, and Collaborative Innovation Center for Biotherapy, No. 37 Guoxue Alley, Wuhou District, Chengdu, Sichuan 610041, China.
Gaoxing LuoInstitute of Burn Research, State Key Laboratory of Trauma and Chemical Poisoning, the First Affiliated Hospital of Army Medical University (the Third Military Medical University), 30 Gaotanyan Main Street, Shapingba District, Chongqing 400038, China.
Weifeng HeInstitute of Burn Research, State Key Laboratory of Trauma and Chemical Poisoning, the First Affiliated Hospital of Army Medical University (the Third Military Medical University), 30 Gaotanyan Main Street, Shapingba District, Chongqing 400038, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Wound healing is a sophisticated biological process characterized by the orchestrated interplay of diverse cellular components, growth factors, and signaling cascades. Recent research has highlighted the pivotal role of fibroblast exosomes in mediating intercellular communication and facilitating tissue regeneration. This investigation aimed to elucidate the therapeutic efficacy of fibroblast exosomes in enhancing wound repair mechanisms, with a particular emphasis on their differential effects in normal and diabetic wound healing paradigms. Methods: A mouse full-thickness skin defect model was used to evaluate the effects of fibroblast exosomes on wound re-epithelialization, granulation tissue formation, and epidermal barrier function. Molecular and cellular experiments were conducted to analyze the roles of exosomes in epidermal stem cell proliferation, migration, differentiation, and antioxidant stress, with further validation of the associated signaling pathways. The therapeutic efficacy was additionally confirmed in a type 1 diabetic mouse model. Results: Fibroblast exosomes significantly enhanced wound re-epithelialization by promoting the proliferation, migration, and differentiation of epidermal stem cells. Additionally, exosomes increased fibroblast abundance and myofibroblast activation, facilitating granulation tissue formation as well as improving extracellular matrix (ECM) deposition and the biomechanical properties of healed skin. Furthermore, exosomes improved epidermal barrier function by upregulating tight junction proteins (e.g. Claudin-1 and ZO-1) and reducing transepidermal water loss (TEWL). In diabetic mouse models, exosomes accelerated wound closure, restored ECM deposition and biomechanical integrity, and repaired epidermal barrier function. Mechanistically, exosomes target the 3' untranslated region (UTR) of Keap1 mRNA through miR-29a-3p and activate the KEAP1/Nrf2 antioxidant pathway, mitigating oxidative stress and protecting epidermal stem cells from reactive oxygen species (ROS)-induced damage. Conclusion: Fibroblast exosomes alleviate oxidative damage by modulating the KEAP1/Nrf2 pathway through miR-29a-3p and enhancing epidermal stem cell function. These exosomes exhibit remarkable therapeutic potential in accelerating wound healing and improving healing quality under both normal and diabetic conditions, offering a robust foundation for innovative therapeutic strategies.

Indexed as

Biomechanical integrityEpidermal barrierFibroblast exosomesKEAP1/Nrf2 pathwayWound healing

Identifiers

PMID41146891
PMCPMC12554163

What OpenQuestion holds

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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.