Evidence map›Paper›PMID 41491569›Full record

ArticleStem cell research & therapy2026

Mesenchymal stromal cells alleviate pulmonary arterial hypertension by suppressing pulmonary arterial adventitial fibroblast activation and extracellular matrix remodeling via the SOCS3/STAT3 pathway.

Jiaojiao Wang, Jing Jin, Mengni Zhang, Xinyuan Chen, Sheng Du, Xiaoxiao Mao, Changlei Bao, Jinsheng Zhu, Xinyu Song, Shiyue Li

Abstract read
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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

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2 · The registry

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3 · Its place in the literature

Who cites it

1 citing paper in PubMed.

  1. Review
4 · The record

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5 · Who and what money

Authors and funding

10 authors.

Jiaojiao Wang *Department of Respiratory and Critical Care Medicine, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Jing Jin *State Key Laboratory of Respiratory Disease, National Center for Respiratory Medicine, Guangzhou Institute of Respiratory Health, National Clinical Research Center for Respiratory Disease, the First Affiliated Hospital of Guangzhou Medical University, Guangzhou, China.
Mengni ZhangState Key Laboratory of Respiratory Disease, National Center for Respiratory Medicine, Guangzhou Institute of Respiratory Health, National Clinical Research Center for Respiratory Disease, the First Affiliated Hospital of Guangzhou Medical University, Guangzhou, China.
Xinyuan ChenState Key Laboratory of Respiratory Disease, National Center for Respiratory Medicine, Guangzhou Institute of Respiratory Health, National Clinical Research Center for Respiratory Disease, the First Affiliated Hospital of Guangzhou Medical University, Guangzhou, China.
Sheng DuState Key Laboratory of Respiratory Disease, National Center for Respiratory Medicine, Guangzhou Institute of Respiratory Health, National Clinical Research Center for Respiratory Disease, the First Affiliated Hospital of Guangzhou Medical University, Guangzhou, China.
Xiaoxiao MaoState Key Laboratory of Respiratory Disease, National Center for Respiratory Medicine, Guangzhou Institute of Respiratory Health, National Clinical Research Center for Respiratory Disease, the First Affiliated Hospital of Guangzhou Medical University, Guangzhou, China.
Changlei BaoState Key Laboratory of Respiratory Disease, National Center for Respiratory Medicine, Guangzhou Institute of Respiratory Health, National Clinical Research Center for Respiratory Disease, the First Affiliated Hospital of Guangzhou Medical University, Guangzhou, China.
Jinsheng ZhuState Key Laboratory of Respiratory Disease, National Center for Respiratory Medicine, Guangzhou Institute of Respiratory Health, National Clinical Research Center for Respiratory Disease, the First Affiliated Hospital of Guangzhou Medical University, Guangzhou, China.
Xinyu SongState Key Laboratory of Respiratory Disease, National Center for Respiratory Medicine, Guangzhou Institute of Respiratory Health, National Clinical Research Center for Respiratory Disease, the First Affiliated Hospital of Guangzhou Medical University, Guangzhou, China. songxinyu@gzhmu.edu.cn.
Shiyue LiDepartment of Respiratory and Critical Care Medicine, Nanfang Hospital, Southern Medical University, Guangzhou, China. lishiyue@gird.cn.

Funding

Guangdong Key Area R&D Program Key Project 2023B111105006Guangzhou fundamental and Basic Fundamental Projects 2025A04J3626National Natural Science Foundation of China 82203883National Science and Technology Major Project 2024ZD0522600
6 · The paper itself

Abstract

backgroundPulmonary arterial hypertension (PAH) is a fatal condition characterized by progressive vascular remodeling in the pulmonary arteries, eventually leading to right heart failure and death. Dysregulated extracellular matrix (ECM) remodeling is central to PAH pathogenesis and represents a potential therapeutic target. Mesenchymal stromal cells (MSCs) have shown promise in preclinical studies; however, the optimal therapeutic window, dosing frequency, and mechanistic basis for their regulation of vascular ECM remain unclear.

methodsWe employed a monocrotaline (MCT)-induced rat model of PAH to evaluate different MSC treatment regimens, including early administration (day 1 post-MCT), delayed administration (days 7 and 14), and repeated dosing (days 1 and 11). Additionally, we combined in vivo and in vitro approaches to investigate how MSCs modulate the activation of pulmonary arterial adventitial fibroblasts (PAAFs) and influence ECM remodeling.

resultsBiodistribution studies indicated that MSC retention in lung tissue peaked within 24 h and gradually declined by day 21. A single early dose of MSCs (on day 1) significantly ameliorated PAH progression, increasing the 28-day survival rate, reducing right ventricular systolic pressure (RVSP), improving right ventricular function, and attenuating small pulmonary vascular remodeling, including reductions in medial thickening, excessive muscularization, and collagen deposition. Repeated MSC administration did not provide additive therapeutic benefit. Both in animal models and cell cultures, MSCs effectively suppressed PAAF activation and reduced ECM protein production. This anti-fibrotic effect was mediated, at least in part, via the pathway involving the upregulation of SOCS3 and consequent inhibition of STAT3 phosphorylation.

conclusionOur findings underscore the importance of early intervention in the PAH disease course for MSC-based therapy. MSCs attenuate vascular remodeling and disease progression, possibly through the SOCS3/STAT3 signaling pathway, by targeting PAAF activation and ECM dysregulation. These results offer a novel mechanistic foundation for MSC treatment in PAH.

Indexed as

Extracellular MatrixFibroblastsHypertension, PulmonaryMesenchymal Stem CellsMesenchymal Stem Cell TransplantationPulmonary Arterial HypertensionPulmonary ArterySTAT3 Transcription FactorSuppressor of Cytokine Signaling 3 ProteinAdventitiaAnimalsDisease Models, AnimalMaleMonocrotalineRatsRats, Sprague-DawleyMonocrotalineSocs3 protein, ratStat3 protein, ratSTAT3 Transcription FactorSuppressor of Cytokine Signaling 3 ProteinExtracellular matrixFibroblastsMesenchymal stromal cellsPulmonary arterial hypertensionSOCS3/STAT3 pathway

Identifiers

PMID41491569
PMCPMC12871029

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LicenceCC BY-NC-ND
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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.