Evidence map›Paper›PMID 26113441›Full record

ArticleExperimental & molecular medicine2015

Emodin prevents intima thickness via Wnt4/Dvl-1/β-catenin signaling pathway mediated by miR-126 in balloon-injured carotid artery rats.

Jun-yi Hua, Yu-zhou He, Yun Xu, Xu-hong Jiang, Wu Ye, Zhi-min Pan

Open access · goldAbstract read
In one paragraph

Article in Experimental & molecular medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.7field-weighted citation impact, top 17% of its field
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

18 citing papers in PubMed, 28 citations in OpenAlex.

  1. Cardioprotective Effects ofLife (Basel, Switzerland) · 2026
    Review
  2. Review
  3. Article
  4. Article
  5. Micro-Executor of Natural Products in Metabolic Diseases.Molecules (Basel, Switzerland) · 2023
    Review
  6. Article
  7. BioMed research international · 2021
    Article
  8. Article
  9. Article
  10. Review
  11. Emodin protects H9c2 cells from hypoxia-induced injury by up-regulating miR-138 expression.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2019
    Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. 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

6 authors at 2 institutions in 1 country.

Jun-yi HuaDepartment of Cardiology, The First Affiliated Hospital, Zhejiang University of Traditional Chinese Medicine, Hangzhou, China.
Yu-zhou HeDepartment of Cardiology, The First Affiliated Hospital, Zhejiang University of Traditional Chinese Medicine, Hangzhou, China.
Yun XuDepartment of Cardiology, The First Affiliated Hospital, Zhejiang University of Traditional Chinese Medicine, Hangzhou, China.
Xu-hong JiangDepartment of Cardiology, The First Affiliated Hospital, Zhejiang University of Traditional Chinese Medicine, Hangzhou, China.
Wu YeDepartment of Cardiology, The First Affiliated Hospital, Zhejiang University of Traditional Chinese Medicine, Hangzhou, China.
Zhi-min PanDepartment of Cardiology, The First Affiliated Hospital, Zhejiang University of Traditional Chinese Medicine, Hangzhou, China.
First Affiliated Hospital Zhejiang University · CNZhejiang Chinese Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Neointimal proliferation after vascular injury is a key mechanism of restenosis, a major cause of percutaneous transluminal angioplasty failure and artery bypass occlusion. Emodin, an anthraquinone with multiple physiological activities, has been reported to inhibit proliferation of vascular smooth muscle cells (VSMCs) that might cause intimal arterial thickening. Thus, in this study, we established a rat model of balloon-injured carotid artery and investigated the therapeutic effect of emodin and its underlying mechanism. Intimal thickness was analyzed by hematoxylin and eosin staining. Expression of Wnt4, dvl-1, β-catenin and collagen was determined by immunohistochemistry and/or western blotting. The proliferation of VSMC was evaluated by MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide) assay and electron microscopy. MicroRNA levels were quantified by real-time quantitative PCR. Emodin relieved injury-induced artery intimal thickness. Results of western blots and immunohistochemistry showed that emodin suppressed expression of signaling molecules Wnt4/Dvl-1/β-catenin as well as collagen protein in the injured artery. In addition, emodin enhanced expression of an artery injury-related microRNA, miR-126. In vitro, MTT assay showed that emodin suppressed angiotensin II (AngII)-induced proliferation of VSMCs. Emodin reversed AngII-induced activation of Wnt4/Dvl-1/β-catenin signaling by increasing expression of miR-126 that was strongly supported by transfection of mimic or inhibitor for miR-126. Emodin prevents intimal thickening via Wnt4/Dvl-1/β-catenin signaling pathway mediated by miR-126 in balloon-injured carotid artery of rats.

Indexed as

Adaptor Proteins, Signal TransducingAnimalsbeta CateninCarotid ArteriesCarotid Artery InjuriesCell ProliferationDishevelled ProteinsEmodinMaleMicroRNAsPhosphoproteinsRatsRats, Sprague-DawleySignal TransductionTunica IntimaWnt4 ProteinAdaptor Proteins, Signal Transducingbeta CateninDishevelled ProteinsDvl1 protein, ratEmodinMicroRNAsMIRN126 microRNA, ratPhosphoproteinsWnt4 Protein

Identifiers

PMID26113441
PMCPMC4491726
OpenAlexW1493615373

What OpenQuestion holds

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LicenceCC BY-NC-ND
Read underepoch 390

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.