Evidence map›Paper›PMID 23533637›Full record

ArticlePloS one2013

Salvianolic acid A, a novel matrix metalloproteinase-9 inhibitor, prevents cardiac remodeling in spontaneously hypertensive rats.

Baohong Jiang, Defang Li, Yanping Deng, Fukang Teng, Jing Chen, Song Xue, Xiangqian Kong, Cheng Luo, Xu Shen, Hualiang Jiang and 8 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed, 1 pooled it
5.9field-weighted citation impact, top 3% 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

32 citing papers in PubMed, 1 synthesis or guideline pooled it, 71 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Review
  4. Article
  5. Review
  6. Review
  7. Article
  8. Article
  9. Cardiovascular & hematological agents in medicinal chemistry · 2023
    Article
  10. Medicinal Plants in the Treatment of Hypertension: A Review.Advanced pharmaceutical bulletin · 2021
    Review
  11. Activated PKB/GSK-3Acta pharmaceutica Sinica. B · 2021
    Article
  12. MMP9 inhibition increases autophagic flux in chronic heart failure.American journal of physiology. Heart and circulatory physiology · 2020
    Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Review
  20. 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

18 authors at 4 institutions in 1 country.

Baohong JiangShanghai Institute of Materia Medica, Chinese Academy of Sciences, Shanghai, China. jiangbh@mail.shcnc.ac.cn
Defang Li
Yanping Deng
Fukang Teng
Jing Chen
Song Xue
Xiangqian Kong
Cheng Luo
Xu Shen
Hualiang Jiang
Feng Xu
Wengang Yang
Jun Yin
Yanhui Wang
Hui Chen
Wanying Wu
Xuan Liu
De-an Guo
Shanghai Institute of Materia Medica · CNChinese Academy of Sciences · CNRenji Hospital · CNShenyang Pharmaceutical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cardiac fibrosis is a deleterious consequence of hypertension which may further advance to heart failure and increased matrix metalloproteinase-9 (MMP-9) contributes to the underlying mechanism. Therefore, new therapeutic strategies to attenuate the effects of MMP-9 are urgently needed. In the present study, we characterize salvianolic acid A (SalA) as a novel MMP-9 inhibitor at molecular, cellular and animal level. We expressed a truncated form of MMP-9 which contains only the catalytic domain (MMP-9 CD), and used this active protein for enzymatic kinetic analysis and Biacore detection. Data generated from these assays indicated that SalA functioned as the strongest competitive inhibitor of MMP-9 among 7 phenolic acids from Salvia miltiorrhiza. In neonatal cardiac fibroblast, SalA inhibited fibroblast migration, blocked myofibroblast transformation, inhibited secretion of intercellular adhesion molecule (ICAM), interleukin-6 (IL-6) and soluble vascular cell adhesion molecule-1 (sVCAM-1) as well as collagen induced by MMP-9 CD. Functional effects of SalA inhibition on MMP-9 was further confirmed in cultured cardiac H9c2 cell overexpressing MMP-9 in vitro and in heart of spontaneously hypertensive rats (SHR) in vivo. Moreover, SalA treatment in SHR resulted in decreased heart fibrosis and attenuated heart hypertrophy. These results indicated that SalA is a novel inhibitor of MMP-9, thus playing an inhibitory role in hypertensive fibrosis. Further studies to develop SalA and its analogues for their potential clinical application of cardioprotection are warranted.

Indexed as

AnimalsAnimals, NewbornCaffeic AcidsCell LineCell MovementCell ProliferationCells, CulturedHypertensionLactatesMaleMatrix Metalloproteinase 9Matrix Metalloproteinase InhibitorsRatsRats, Inbred SHRCaffeic AcidsLactatesMatrix Metalloproteinase 9Matrix Metalloproteinase Inhibitorssalvianolic acid A

Identifiers

PMID23533637
PMCPMC3606118
OpenAlexW2007939201

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.