Evidence map›Paper›PMID 41794821›Full record

ArticleNature communications2026

Perivascular mesenchymal cells instruct ST2+ reparative macrophages to promote endovascular injury-induced neointimal hyperplasia in mice.

Yan Ping, Zhewen Qin, Xingxiao Huang, Qiuli Sun, Tao Yao, Siqi Li, Xin Tian, Xintong Xia, Bowen Diao, Lin Zhao and 7 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Nature communications, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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.

Yan PingZhejiang Key Laboratory of Pancreatic Disease, The First Affiliated Hospital, Zhejiang Key Laboratory of Frontier Medical Research on Cancer Metabolism, and Institute of Translational Medicine, Zhejiang University School of Medicine, Hangzhou, Zhejiang, China.
Zhewen QinZhejiang Key Laboratory of Pancreatic Disease, The First Affiliated Hospital, Zhejiang Key Laboratory of Frontier Medical Research on Cancer Metabolism, and Institute of Translational Medicine, Zhejiang University School of Medicine, Hangzhou, Zhejiang, China.
Xingxiao HuangZhejiang Key Laboratory of Pancreatic Disease, The First Affiliated Hospital, Zhejiang Key Laboratory of Frontier Medical Research on Cancer Metabolism, and Institute of Translational Medicine, Zhejiang University School of Medicine, Hangzhou, Zhejiang, China.
Qiuli SunZhejiang Key Laboratory of Pancreatic Disease, The First Affiliated Hospital, Zhejiang Key Laboratory of Frontier Medical Research on Cancer Metabolism, and Institute of Translational Medicine, Zhejiang University School of Medicine, Hangzhou, Zhejiang, China.
Tao YaoZhejiang Key Laboratory of Pancreatic Disease, The First Affiliated Hospital, Zhejiang Key Laboratory of Frontier Medical Research on Cancer Metabolism, and Institute of Translational Medicine, Zhejiang University School of Medicine, Hangzhou, Zhejiang, China.
Siqi LiUniversity of Chinese Academy of Sciences, Beijing, China.
Xin TianZhejiang Key Laboratory of Pancreatic Disease, The First Affiliated Hospital, Zhejiang Key Laboratory of Frontier Medical Research on Cancer Metabolism, and Institute of Translational Medicine, Zhejiang University School of Medicine, Hangzhou, Zhejiang, China.
Xintong XiaTongde Hospital of Zhejiang Province, Zhejiang Chinese Medical University, Hangzhou, Zhejiang, China.
Bowen DiaoZhejiang Key Laboratory of Pancreatic Disease, The First Affiliated Hospital, Zhejiang Key Laboratory of Frontier Medical Research on Cancer Metabolism, and Institute of Translational Medicine, Zhejiang University School of Medicine, Hangzhou, Zhejiang, China.
Lin ZhaoZhejiang Key Laboratory of Pancreatic Disease, The First Affiliated Hospital, Zhejiang Key Laboratory of Frontier Medical Research on Cancer Metabolism, and Institute of Translational Medicine, Zhejiang University School of Medicine, Hangzhou, Zhejiang, China.
Xinyuan ZhangSchool of Basic Medical Sciences and Forensic Medicine, Hangzhou Medical College, Hangzhou, Zhejiang, China.
Danni WeiUniversity of Chinese Academy of Sciences, Beijing, China.
Long WangDepartment of Cardiology, Westlake laboratory of Life Sciences and Biomedicine, Affiliated Hangzhou First People's Hospital, Westlake University School of Medicine, Hangzhou, Zhejiang, China.
Mengle ShaoKey Laboratory of Immune Response and Immunotherapy, Shanghai Institute of Immunity and Infection, Chinese Academy of Sciences, Shanghai, China. mlshao@ips.ac.cn.ORCID http://orcid.org/0000-0002-5488-9904
Ying WuTongde Hospital of Zhejiang Province, Zhejiang Chinese Medical University, Hangzhou, Zhejiang, China. wuying@sibs.ac.cn.ORCID http://orcid.org/0009-0008-1808-3349
Jinyu HuangDepartment of Cardiology, Westlake laboratory of Life Sciences and Biomedicine, Affiliated Hangzhou First People's Hospital, Westlake University School of Medicine, Hangzhou, Zhejiang, China. zdsyhjy0902@zju.edu.cn.
Bo ShanZhejiang Key Laboratory of Pancreatic Disease, The First Affiliated Hospital, Zhejiang Key Laboratory of Frontier Medical Research on Cancer Metabolism, and Institute of Translational Medicine, Zhejiang University School of Medicine, Hangzhou, Zhejiang, China. boshan@zju.edu.cn.ORCID http://orcid.org/0000-0002-1675-5809

Funding

National Natural Science Foundation of China (National Science Foundation of China) 32371235National Natural Science Foundation of China (National Science Foundation of China) 32571287
6 · The paper itself

Abstract

Tissue-resident mesenchymal stromal cells (MSC) instruct immune cell activation at injury sites, a key event in tissue repair. However, the full array of immunomodulatory mechanisms driving injury-responsive immune-stromal cell interactions is underexplored. Here, using an endovascular injury mouse model, we demonstrate that perivascular MSCs enhance arterial immune response by facilitating recruitment of ST2-expressing reparative macrophages in male mice. Time-resolved single-cell sequencing reveals an MSC-mediated, macrophage phenotypic switch, essential for vascular regeneration. Mechanistically, injury activates NFκB-dependent IL-33 production in MSCs, which acts as a paracrine signal that drives Osteopontin (OPN/SPP1) production in ST2+ macrophages and stimulates vascular smooth muscle cell (VSMC) proliferation and neointima formation. Local hydrogel-mediated delivery of siRNAs targeting Il33 or Spp1 effectively alleviates injury-induced neointimal hyperplasia, suggesting a potential therapeutic strategy to prevent restenosis and other vascular diseases. Our findings define an IL33-ST2-OPN axis that mediates functional crosstalk between perivascular MSCs and reparative macrophages, orchestrating immune-mediated reparative responses.

Indexed as

Interleukin-1 Receptor-Like 1 ProteinMacrophagesMesenchymal Stem CellsNeointimaAnimalsCell ProliferationDisease Models, AnimalHyperplasiaInterleukin-33MaleMiceMice, Inbred C57BLMuscle, Smooth, VascularMyocytes, Smooth MuscleNF-kappa BOsteopontinIl1rl1 protein, mouseIl33 protein, mouseInterleukin-1 Receptor-Like 1 ProteinInterleukin-33NF-kappa BOsteopontinRNA, Small InterferingSpp1 protein, mouse

Identifiers

PMID41794821
PMCPMC13096279

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.