Evidence map›Paper›PMID 25793583›Full record

ArticlePloS one2015

Suppression of TGF-β1/Smad signaling pathway by sesamin contributes to the attenuation of myocardial fibrosis in spontaneously hypertensive rats.

Mengqiu Zhao, Shuguo Zheng, Jieren Yang, Yuanjie Wu, Younan Ren, Xiang Kong, Wei Li, Jiali Xuan

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
9.8field-weighted citation impact, top 2% 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

19 citing papers in PubMed, 42 citations in OpenAlex.

  1. Article
  2. Article
  3. Effects of sesame (Food science & nutrition · 2023
    Review
  4. Article
  5. Article
  6. Review
  7. Review
  8. Article
  9. Article
  10. Article
  11. Regulatory Effect of 1,25(OH)2D3 on TGF-International journal of endocrinology · 2019
    Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Review
  18. Article
  19. 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

8 authors at 2 institutions in 1 country.

Mengqiu ZhaoDepartment of Pharmacology, Wannan Medical College, Wuhu, 241002, China.
Shuguo ZhengDepartment of Pharmacology, Wannan Medical College, Wuhu, 241002, China.
Jieren YangDepartment of Pharmacology, Wannan Medical College, Wuhu, 241002, China.
Yuanjie WuDepartment of Basic Theory of Chinese Medicine, Anhui University of Chinese Medicine, Hefei, 230038, China.
Younan RenDepartment of Pharmacology, Wannan Medical College, Wuhu, 241002, China.
Xiang KongDepartment of Pharmacology, Wannan Medical College, Wuhu, 241002, China.
Wei LiDepartment of Pharmacology, Wannan Medical College, Wuhu, 241002, China.
Jiali XuanDepartment of Pharmacology, Wannan Medical College, Wuhu, 241002, China.
Wannan Medical College · CNAnhui University of Traditional Chinese Medicine · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

This study investigated the effect of sesamin on myocardial fibrosis in spontaneously hypertensive rats (SHRs) and the possible mechanisms involved. Twenty-eight male SHRs were randomly allocated to SHR group, Ses160 group (sesamin 160 mg/kg), Ses80 group (sesamin 80 mg/kg) and Cap30 group (captopril 30 mg/kg). Seven male WKY rats were used as control. Sesamin and captopril were administered intragastrically for 12 weeks. Captopril significantly reduced systolic blood pressure and angiotensin II (Ang II) levels in SHRs, accompanied by a marked attenuation of left ventricular hypertrophy (LVH) and collagen deposition (P <0.05 or P <0.01). Though sesamin had no significant influence on Ang II levels, and the hypotensive effect was also significantly inferior to that of captopril (P <0.05 or P <0.01), however, the improvement of LVH and collagen deposition was similar to that in captopril group. Sesamin markedly reduced transforming growth factor-β1 (TGF-β1) content in cardiac tissues, with Smad3 phosphorylation decreased and Smad7 protein expression increased notably (P <0.05 or P <0.01). Protein expression of type I collagen and type III collagen, target genes of Smad3, was down-regulated markedly by sesamin (P <0.05 or P <0.01). In addition, sesamin significantly increased total antioxidant capacity and superoxide dismutase protein in cardiac tissues (P <0.05 or P <0.01), while the expression of NADPH oxidase subunit p47phox and malondialdehyde content were reduced markedly (P <0.05 or P <0.01). In vitro studies also demonstrated that sesamin was able to suppress Ang II induced phosphorylation of Smad3 and secretion of TGF-β1 and type I and type III collagen in cultured rat cardiac fibroblasts. These data suggest that sesamin is capable of attenuating hypertensive myocardial fibrosis through, at least partly, suppression of TGF-β1/Smad signaling pathway.

Indexed as

Angiotensin IIAnimalsAntioxidantsBlood PressureCollagen Type ICollagen Type IIIDioxolesFibroblastsFibrosisHeart VentriclesLignansMaleMalondialdehydeMyocardiumNADPH OxidasesOrgan SizeAngiotensin IIAntioxidantsCollagen Type ICollagen Type IIIDioxolesLignansMalondialdehydeNADPH Oxidasesneutrophil cytosolic factor 1sesaminSmad3 ProteinSmad7 ProteinSuperoxide DismutaseTransforming Growth Factor beta1

Identifiers

PMID25793583
PMCPMC4368740
OpenAlexW2101251935

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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.