Evidence map›Paper›PMID 41617709›Full record

ArticleNature communications2026

Tenascin C

Xinran Tong, Guangzheng Shi, Zilong Fang, Sibei Tang, Bin Zhou, Qingyou Meng, Peili Zhang, Haixiang Li, Xiaojie Cai, Zhikai Wang and 6 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. 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

16 authors.

Xinran Tong *The Department of Cardiovascular Medicine, State Key Laboratory of Medical Genomics, Shanghai Key Laboratory of Hypertension, Ruijin Hospital, Shanghai Institute of Hypertension, Shanghai Jiao Tong University School of Medicine, 197 Ruijin 2nd Road, Shanghai, China.ORCID 0009-0002-1456-2517
Guangzheng Shi *The Department of Cardiovascular Medicine, State Key Laboratory of Medical Genomics, Shanghai Key Laboratory of Hypertension, Ruijin Hospital, Shanghai Institute of Hypertension, Shanghai Jiao Tong University School of Medicine, 197 Ruijin 2nd Road, Shanghai, China.
Zilong Fang *The Department of Cardiovascular Medicine, State Key Laboratory of Medical Genomics, Shanghai Key Laboratory of Hypertension, Ruijin Hospital, Shanghai Institute of Hypertension, Shanghai Jiao Tong University School of Medicine, 197 Ruijin 2nd Road, Shanghai, China.
Sibei TangPrecision Research Center for Refractory Diseases, Institute for Clinical Research, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Bin ZhouCAS CEMCS-CUHK Joint Laboratories, New Cornerstone Science Laboratory, Key Laboratory of Multi-Cell Systems, Shanghai Institute of Biochemistry and Cell Biology, Center for Excellence in Molecular Cell Science, Chinese Academy of Sciences, University of Chinese Academy of Sciences, Shanghai, China.ORCID 0000-0001-5278-5522
Qingyou MengDepartment of Vascular Surgery, General Surgery Clinical Center, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Peili ZhangThe Department of Cardiovascular Medicine, State Key Laboratory of Medical Genomics, Shanghai Key Laboratory of Hypertension, Ruijin Hospital, Shanghai Institute of Hypertension, Shanghai Jiao Tong University School of Medicine, 197 Ruijin 2nd Road, Shanghai, China.
Haixiang LiDepartment of Vascular Surgery, General Surgery Clinical Center, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Xiaojie CaiPrecision Research Center for Refractory Diseases, Institute for Clinical Research, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.ORCID 0000-0001-7297-4865
Zhikai WangPrecision Research Center for Refractory Diseases, Institute for Clinical Research, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Xichen ZhengPrecision Research Center for Refractory Diseases, Institute for Clinical Research, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Wendong ChenThe Department of Cardiovascular Medicine, State Key Laboratory of Medical Genomics, Shanghai Key Laboratory of Hypertension, Ruijin Hospital, Shanghai Institute of Hypertension, Shanghai Jiao Tong University School of Medicine, 197 Ruijin 2nd Road, Shanghai, China.
Gonghao JiangThe Department of Cardiovascular Medicine, State Key Laboratory of Medical Genomics, Shanghai Key Laboratory of Hypertension, Ruijin Hospital, Shanghai Institute of Hypertension, Shanghai Jiao Tong University School of Medicine, 197 Ruijin 2nd Road, Shanghai, China.
Honglin WangPrecision Research Center for Refractory Diseases, Institute for Clinical Research, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China. honglin.wang@sjtu.edu.cn.
Dongsheng JiangPrecision Research Center for Refractory Diseases, Institute for Clinical Research, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China. dongsheng.jiang@sjtu.edu.cn.ORCID 0000-0003-0961-2671
Qun LiThe Department of Cardiovascular Medicine, State Key Laboratory of Medical Genomics, Shanghai Key Laboratory of Hypertension, Ruijin Hospital, Shanghai Institute of Hypertension, Shanghai Jiao Tong University School of Medicine, 197 Ruijin 2nd Road, Shanghai, China. liqun@sibs.ac.cn.ORCID 0000-0002-0549-1852

Funding

National Natural Science Foundation of China (National Science Foundation of China) 82070509National Natural Science Foundation of China (National Science Foundation of China) 82470432
6 · The paper itself

Abstract

Neointimal hyperplasia (NIH) is a major pathological feature of vascular injury, yet its cellular and molecular drivers remain elusive. Here, using a mouse model of ligation-induced carotid artery NIH, we identify a population of Tenascin C-expressing (Tnc⁺) myofibroblasts (MF). We demonstrate a TNC-driven transition of adventitial fibroblasts (AF) into Tnc⁺ MFs via integrin αvβ1, initiating a positive feedback loop that sustains MF accumulation. In vitro, Tnc⁺ MFs enhance neurite outgrowth, and in vivo, they spatially associate with aberrant axon growth and macrophage accumulation in the perivascular niche. Mechanistically, TNC-activated sensory nerves release CCL2 to recruit macrophages and position them along growing axons. Fibroblast-specific Tnc deletion or sensory neuron inhibition attenuates perivascular hyperinnervation, macrophage recruitment, and neointimal thickening. Importantly, we observe aberrant nerve fibers and macrophage infiltration in human NIH specimens. Thus, we describe a TNC-driven fibroblast-nerve-macrophage axis that sustains inflammation and promotes vascular remodeling. Targeting TNC may offer new therapeutic avenues for vascular diseases.

Indexed as

MacrophagesMyofibroblastsNeointimaTenascinAdventitiaAnimalsCarotid ArteriesDisease Models, AnimalFibroblastsHumansHyperplasiaMaleMiceMice, Inbred C57BLMice, KnockoutSensory Receptor CellsTenascinTnc protein, mouse

Identifiers

PMID41617709
PMCPMC12960667

What OpenQuestion holds

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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 OpenQuestion graph.