Evidence map›Paper›PMID 25132338›Full record

ArticleActa pharmacologica Sinica2014

Curcumin attenuates cardiac fibrosis in spontaneously hypertensive rats through PPAR-γ activation.

Zhe Meng, Xin-hui Yu, Jun Chen, Ling Li, Sheng Li

Abstract read
In one paragraph

Article in Acta pharmacologica Sinica, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
–field-weighted citation impact
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

31 citing papers in PubMed.

  1. Review
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  3. Curcumin in Fibrosis Treatment: A Review.Drug design, development and therapy · 2026
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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

5 authors.

Zhe MengDepartment of Cardiology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou 450052, China.
Xin-hui YuDepartment of Thoracic Surgery, Taicang Affiliated Hospital of Soochow University, Taicang 215400, China.
Jun ChenDepartment of Cardiology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou 450052, China.
Ling LiDepartment of Cardiology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou 450052, China.
Sheng LiDepartment of Thoracic Surgery, Taicang Affiliated Hospital of Soochow University, Taicang 215400, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aimTo investigate the effects of curcumin (Cur) on cardiac fibrosis in spontaneously hypertensive rats (SHRs) and the mechanisms underlying the anti-fibrotic effect of Cur in rat cardiac fibroblasts (CFs) in vitro.

methodsSHRs were orally treated with Cur (100 mg·kg(-1)·d(-1)) or Cur (100 mg·kg(-1)·d(-1)) plus the PPAR-γ antagonist GW9662 (1 mg·kg(-1)·d(-1)) for 12 weeks. Cultured CFs were treated with angiotensin II (Ang II, 0.1 μmol/L) in vitro. The expression of relevant proteins and mRNAs was analyzed using Western blotting and real-time PCR, respectively. The expression and activity of peroxisome proliferator-activated receptor-γ (PPAR-γ) were detected using Western blotting and a DNA-binding assay, respectively.

resultsTreatment of SHRs with Cur significantly decreased systolic blood pressure, blood Ang II concentration, heart weight/body weight ratio and left ventricle weight/body weight ratio, with concurrently decreased expression of connective tissue growth factor (CTGF), plasminogen activator inhibitor (PAI)-1, collagen III (Col III) and fibronectin (FN), and increased expression and activity of PPAR-γ in the left ventricle. Co-treatment with GW9662 partially abrogated the anti-fibrotic effects of Cur in SHRs. Pretreatment of CFs with Cur (5, 10, 20 μmol/L) dose-dependently inhibited Ang II-induced expression of CTGF, PAI-1, Col III and FN, and increased the expression and binding activity of PPAR-γ. Pretreatment with GW9662 partially reversed anti-fibrotic effects of Cur in vitro. Furthermore, pretreatment of CFs with Cur inhibited Ang II-induced expression of transforming growth factor-β1 (TGF-β1) and phosphorylation of Smad2/3, which were reversed by GW9662.

conclusionCur attenuates cardiac fibrosis in SHRs and inhibits Ang II-induced production of CTGF, PAI-1 and ECM in CFs in vitro. The crosstalk between PPAR-γ and TGF-β1/Smad2/3 signaling is involved in the anti-fibrotic and anti-proliferative effects of Cur.

Indexed as

Angiotensin IIAnilidesAnimalsBlood PressureBody WeightCell ProliferationCells, CulturedCollagen Type IIIConnective Tissue Growth FactorCurcuminFibroblastsFibronectinsFibrosisHeart VentriclesMalePlasminogen Activator Inhibitor 12-chloro-5-nitrobenzanilideAngiotensin IIAnilidesCollagen Type IIIConnective Tissue Growth FactorCurcuminFibronectinsPlasminogen Activator Inhibitor 1PPAR gammaSmad2 ProteinSmad2 protein, ratSmad3 ProteinSmad3 protein, ratTransforming Growth Factor beta1

Identifiers

PMID25132338
PMCPMC4186983

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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.