Evidence map›Paper›PMID 40812587›Full record

ArticleJournal of advanced research2026

Airway basal stem cell-derived extracellular vesicles drive ECM remodeling and suppress fibroblasts activation via the miR-30a-5p/FAP axis in benign tracheal stenosis.

Lisi Luo, Junfeng Huang, Difei Chen, Huijie Yang, Yuling Deng, Yushan He, Jinsheng Lin, Ruiyue Zhao, Xinlu Wang, Zhuquan Su and 6 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of advanced research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing 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

5 citing papers in PubMed.

  1. Persistent ZnAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article
  2. Article
  3. Article
  4. Review
  5. Article
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

16 authors.

Lisi LuoGuangzhou Institute of Respiratory Health, State Key Laboratory of Respiratory Disease, National Clinical Research Center for Respiratory Disease, National Center for Respiratory Medicine, the First Affiliated Hospital of Guangzhou Medical University, Guangzhou 510000 Guangdong, China; Guangzhou National Laboratory, No. 9 XingDaoHuanBei Road, Guangzhou International Bio Island, Guangzhou 510005 Guangdong Province, China; Guangzhou Medical University, Guangzhou, Guangdong, China.
Junfeng HuangGuangzhou Institute of Respiratory Health, State Key Laboratory of Respiratory Disease, National Clinical Research Center for Respiratory Disease, National Center for Respiratory Medicine, the First Affiliated Hospital of Guangzhou Medical University, Guangzhou 510000 Guangdong, China; Guangzhou Medical University, Guangzhou, Guangdong, China.
Difei ChenGuangzhou Institute of Respiratory Health, State Key Laboratory of Respiratory Disease, National Clinical Research Center for Respiratory Disease, National Center for Respiratory Medicine, the First Affiliated Hospital of Guangzhou Medical University, Guangzhou 510000 Guangdong, China.
Huijie YangGuangzhou Institute of Respiratory Health, State Key Laboratory of Respiratory Disease, National Clinical Research Center for Respiratory Disease, National Center for Respiratory Medicine, the First Affiliated Hospital of Guangzhou Medical University, Guangzhou 510000 Guangdong, China; Guangzhou Medical University, Guangzhou, Guangdong, China.
Yuling DengGuangzhou Medical University, Guangzhou, Guangdong, China; Department of Nuclear Medicine, The First Affiliated Hospital, Guangzhou Medical University, Guangzhou 510120 Guangdong, China.
Yushan HeGuangzhou Institute of Respiratory Health, State Key Laboratory of Respiratory Disease, National Clinical Research Center for Respiratory Disease, National Center for Respiratory Medicine, the First Affiliated Hospital of Guangzhou Medical University, Guangzhou 510000 Guangdong, China; Guangzhou Medical University, Guangzhou, Guangdong, China.
Jinsheng LinGuangzhou Institute of Respiratory Health, State Key Laboratory of Respiratory Disease, National Clinical Research Center for Respiratory Disease, National Center for Respiratory Medicine, the First Affiliated Hospital of Guangzhou Medical University, Guangzhou 510000 Guangdong, China; Guangzhou Medical University, Guangzhou, Guangdong, China.
Ruiyue ZhaoDepartment of Nuclear Medicine, The First Affiliated Hospital, Guangzhou Medical University, Guangzhou 510120 Guangdong, China.
Xinlu WangDepartment of Nuclear Medicine, The First Affiliated Hospital, Guangzhou Medical University, Guangzhou 510120 Guangdong, China.
Zhuquan SuGuangzhou Institute of Respiratory Health, State Key Laboratory of Respiratory Disease, National Clinical Research Center for Respiratory Disease, National Center for Respiratory Medicine, the First Affiliated Hospital of Guangzhou Medical University, Guangzhou 510000 Guangdong, China.
Huanjie ChenGuangzhou Institute of Respiratory Health, State Key Laboratory of Respiratory Disease, National Clinical Research Center for Respiratory Disease, National Center for Respiratory Medicine, the First Affiliated Hospital of Guangzhou Medical University, Guangzhou 510000 Guangdong, China.
Minting WuGuangzhou Institute of Respiratory Health, State Key Laboratory of Respiratory Disease, National Clinical Research Center for Respiratory Disease, National Center for Respiratory Medicine, the First Affiliated Hospital of Guangzhou Medical University, Guangzhou 510000 Guangdong, China.
Yingying GuGuangzhou Institute of Respiratory Health, State Key Laboratory of Respiratory Disease, National Clinical Research Center for Respiratory Disease, National Center for Respiratory Medicine, the First Affiliated Hospital of Guangzhou Medical University, Guangzhou 510000 Guangdong, China.
Zhucheng ChenGuangzhou Institute of Respiratory Health, State Key Laboratory of Respiratory Disease, National Clinical Research Center for Respiratory Disease, National Center for Respiratory Medicine, the First Affiliated Hospital of Guangzhou Medical University, Guangzhou 510000 Guangdong, China.
Ning MaGuangzhou National Laboratory, No. 9 XingDaoHuanBei Road, Guangzhou International Bio Island, Guangzhou 510005 Guangdong Province, China; Guangzhou Medical University, Guangzhou, Guangdong, China. Electronic address: ma_ning@gzlab.ac.cn.
Shiyue LiGuangzhou Institute of Respiratory Health, State Key Laboratory of Respiratory Disease, National Clinical Research Center for Respiratory Disease, National Center for Respiratory Medicine, the First Affiliated Hospital of Guangzhou Medical University, Guangzhou 510000 Guangdong, China. Electronic address: lishiyue@gzhmu.edu.cn.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionBenign tracheal stenosis (BTS) is characterized by granulation tissue hyperplasia, driven by abnormal fibroblast activation and excessive extracellular matrix deposition. Targeting these mechanisms with novel therapies may offer a promising approach to addressing or preventing re-stenosis. Our previous study demonstrated that airway basal stem cell (BSC) transplantation can inhibit granulation hyperplasia in BTS.

objectivesGiven the therapeutic potential of extracellular vesicles (EVs) as mediators in cell-based therapies, we investigated the in vivo efficacy of airway BSC-derived EVs (BSC-EVs) and explored their underlying mechanisms.

methodsBTS was induced in rabbits via tracheal mucosal injury. BSC-EVs were isolated, characterized, and intratracheally delivered. Then, therapeutic effects were evaluated using bronchoscopy,

resultsOur findings revealed that BSC-EVs significantly reduce granulation hyperplasia, promote ECM remodeling and improve collagen fiber alignment, leading to enhanced airway patency and prolonged survival. Mechanistically, we identified miR-30a-5p as a key functional cargo within BSC-EVs, which directly targets the fibroblast activation protein (FAP) gene. In vitro experiments demonstrated that miR-30a-5p mediates the anti-fibrotic effects of BSC-EVs by attenuating fibroblast activation, collagen contraction, and ECM deposition.

conclusionsThese findings suggest that BSC-EVs represent a promising therapeutic strategy for BTS by inhibiting fibroblast activation and promoting ECM remodeling via the miR-30a-5p/FAP axis, offering a novel advancement beyond current treatment approaches.

Indexed as

Extracellular MatrixExtracellular VesiclesFibroblastsMembrane ProteinsMicroRNAsStem CellsTracheal StenosisAnimalsDisease Models, AnimalHumansMaleRabbitsMembrane ProteinsMicroRNAsMIRN30a microRNA, humanAirway basal stem cellBenign tracheal stenosisExcessive extracellular matrix depositionExtracellular vesiclesFibroblast activation

Identifiers

PMID40812587
PMCPMC13131431

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
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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.