Evidence map›Paper›PMID 29367637›Full record

ArticleCell death & disease2018

Rosmarinic acid attenuates cardiac fibrosis following long-term pressure overload via AMPKα/Smad3 signaling.

Xin Zhang, Zhen-Guo Ma, Yu-Pei Yuan, Si-Chi Xu, Wen-Ying Wei, Peng Song, Chun-Yan Kong, Wei Deng, Qi-Zhu Tang

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 papers.

0numbers the graph read from it
0cells of the map it votes in
68citing papers in PubMed
11.1field-weighted citation impact, top 1% 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

68 citing papers in PubMed, 135 citations in OpenAlex.

  1. Review
  2. Article
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  8. Article
  9. Inhibition of AMPKα Pathway by Podocyte GOLM1 Exacerbates Diabetic Nephrology in Mice.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Frontiers in pharmacology · 2025
    Review
  15. Effects of aNutrients · 2024
    Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Review

8 more citing papers are in PubMed but not listed here.

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

9 authors at 2 institutions in 1 country.

Xin ZhangDepartment of Cardiology, Renmin Hospital of Wuhan University, Wuhan, 430060, China.
Zhen-Guo MaDepartment of Cardiology, Renmin Hospital of Wuhan University, Wuhan, 430060, China.
Yu-Pei YuanDepartment of Cardiology, Renmin Hospital of Wuhan University, Wuhan, 430060, China.
Si-Chi XuDepartment of Cardiology, Renmin Hospital of Wuhan University, Wuhan, 430060, China.
Wen-Ying WeiDepartment of Cardiology, Renmin Hospital of Wuhan University, Wuhan, 430060, China.
Peng SongDepartment of Cardiology, Renmin Hospital of Wuhan University, Wuhan, 430060, China.
Chun-Yan KongDepartment of Cardiology, Renmin Hospital of Wuhan University, Wuhan, 430060, China.
Wei DengDepartment of Cardiology, Renmin Hospital of Wuhan University, Wuhan, 430060, China. vivideng1982@whu.edu.cn.
Qi-Zhu TangDepartment of Cardiology, Renmin Hospital of Wuhan University, Wuhan, 430060, China. qztang@whu.edu.cn.
Wuhan University · CNRenmin Hospital of Wuhan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Agonists of peroxisome proliferator-activated receptor gamma (PPAR-γ) can activate 5' AMP-activated protein kinase alpha (AMPKα) and exert cardioprotective effects. A previous study has demonstrated that rosmarinic acid (RA) can activate PPAR-γ, but its effect on cardiac remodeling remains largely unknown. Our study aimed to investigate the effect of RA on cardiac remodeling and to clarify the underlying mechanism. Mice were subjected to aortic banding to generate pressure overload induced cardiac remodeling and then were orally administered RA (100 mg/kg/day) for 7 weeks beginning 1 week after surgery. The morphological examination, echocardiography, and molecular markers were used to evaluate the effects of RA. To ascertain whether the beneficial effect of RA on cardiac fibrosis was mediated by AMPKα, AMPKα2 knockout mice were used. Neonatal rat cardiomyocytes and fibroblasts were separated and cultured to validate the protective effect of RA in vitro. RA-treated mice exhibited a similar hypertrophic response as mice without RA treatment, but had an attenuated fibrotic response and improved cardiac function after pressure overload. Activated AMPKα was essential for the anti-fibrotic effect of RA via inhibiting the phosphorylation and nuclear translocation of Smad3 in vivo and in vitro, and AMPKα deficiency abolished RA-mediated protective effects. Small interfering RNA against Ppar-γ (siPpar-γ) and GW9662, a specific antagonist of PPAR-γ, abolished RA-mediated AMPKα phosphorylation and alleviation of fibrotic response in vitro. RA attenuated cardiac fibrosis following long-term pressure overload via AMPKα/Smad3 signaling and PPAR-γ was required for the activation of AMPKα. RA might be a promising therapeutic agent against cardiac fibrosis.

Indexed as

PressureSignal TransductionAMP-Activated Protein KinasesAnimalsCardiotonic AgentsCell NucleusCell TransdifferentiationCinnamatesDepsidesFibrosisMaleMice, Inbred C57BLMyocardiumPhosphorylationPPAR gammaProtein TransportAMP-Activated Protein KinasesCardiotonic AgentsCinnamatesDepsidesPPAR gammaRosmarinic AcidSmad3 Protein

Identifiers

PMID29367637
PMCPMC5833382
OpenAlexW2794318176

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

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.