Evidence map›Paper›PMID 27677228›Full record

ArticleMedical science monitor : international medical journal of experimental and clinical research2016

Bone Morphogenetic Protein-7 Antagonizes Myocardial Fibrosis Induced by Atrial Fibrillation by Restraining Transforming Growth Factor-β (TGF-β)/Smads Signaling.

Xinjun Chen, Jing Xu, Baozhou Jiang, Danping Liu

Open access · hybridAbstract read
In one paragraph

Article in Medical science monitor : international medical journal of experimental and clinical research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
2.2field-weighted citation impact, top 11% 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

22 citing papers in PubMed, 36 citations in OpenAlex.

  1. Article
  2. Review
  3. Predictive Value of Blood and Echocardiographic Indicators for Nonvalvular Atrial Fibrillation in Postmenopausal Women.Annals of noninvasive electrocardiology : the official journal of the International Society for Holter and Noninvasive Electrocardiology, Inc · 2025
    Article
  4. Review
  5. Therapeutic advances in atrial fibrillation based on animal models.Journal of Zhejiang University. Science. B · 2024
    Review
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  7. Review
  8. Article
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  10. Article
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  16. Article
  17. Article
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  19. Article
  20. The TGFβ superfamily in cardiac dysfunction.Acta biochimica et biophysica Sinica · 2018
    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

4 authors at 3 institutions in 1 country.

Xinjun ChenEmergency Internal Medicine, Shaanxi Province People's Hospital, Xi'an, Shaanxi, China (mainland).
Jing XuDepartment of Emergency, First Affiliated Hospital of Medical College, Xi'an Jiaotong University, Xi'an, Shaanxi, China (mainland).
Baozhou JiangEmergency Internal Medicine, Shaanxi Province People's Hospital, Xi'an, Shaanxi, China (mainland).
Danping LiuEmergency Internal Medicine, Shaanxi Province People's Hospital, Xi'an, Shaanxi, China (mainland).
Shanxi Medical University · CNFirst Affiliated Hospital of Xi'an Jiaotong University · CNShaanxi Provincial People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND This aim of this study was to investigate the expression of BMP-7 in atrial fibrillation and illuminate the role of BMP-7 and TGF-β/Smads signaling in myocardial fibrosis. MATERIAL AND METHODS Fibrosis of myocardial fibroblasts was induced by TGF-β1 and the optimal condition was determined by the MTT assay. Cells with TGF-β1 treatment were sub-divided into 4 groups: TGF-β1 group, TGF-β1 + Smad3 siRNA group, TGF-β1 + BMP-7 group, and TGF-β1 + BMP-7 + Smad1/5 siRNA group. Cells were then analyzed by detecting the expression of epithelial cadherin (E-cadherin), collagen I, alpha smooth muscle cell actin (α-SMA), and activated Smads using Western blot. Mice were injected daily with Ach-CaCl2 with or without the addition of BMP-7 and Smad1/5 siRNA over a period of 4 weeks. Cardiac functions were tested by echocardiogram assay and fibrosis was diagnosed by histopathological examination. Finally, molecule biomarkers were detected using standard procedures. RESULTS TGF-β1 treatment significantly down-regulated E-cadherin expression and up-regulated expressions of Collagen I, α-SMA, and pSmad3 (P<0.05). The effects of TGF-β1 treatment can be significantly suppressed by Smad3 siRNA (P<0.05). Cells in the BMP-7 group exhibited significantly higher expression levels of E-cadherin and pSmad1/5 together with lower expression levels of pSmad3, collagen I, and a-SMA (P<0.05). Moreover, Smad1/5 siRNA can substantially repress the effects of BMP-7 (P<0.05) and results from the mice model coincided with those in myocardial fibroblasts. CONCLUSIONS BMP-7 can regulate TGF-β1/Smad3 by targeting Smad1/5 to antagonize fibrosis in myocardial fibroblasts resulting from atrial fibrillation.

Identifiers

PMID27677228
PMCPMC5045133
OpenAlexW2525287705

What OpenQuestion holds

Textmetadata
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.