Evidence map›Paper›PMID 26648693›Full record

ArticleDrug design, development and therapy2015

Attenuation of myocardial fibrosis with curcumin is mediated by modulating expression of angiotensin II AT1/AT2 receptors and ACE2 in rats.

Xue-Fen Pang, Li-Hui Zhang, Feng Bai, Ning-Ping Wang, Ron E Garner, Robert J McKallip, Zhi-Qing Zhao

Erratum issuedOpen access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Drug design, development and therapy, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 45 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed, 1 pooled it
1.1field-weighted citation impact, top 27% 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

45 citing papers in PubMed, 1 synthesis or guideline pooled it, 81 citations in OpenAlex.

  1. Pooled it
  2. Curcumin in Fibrosis Treatment: A Review.Drug design, development and therapy · 2026
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 2 institutions in 2 countries.

Xue-Fen PangDepartment of Physiology, Shanxi Medical University, Taiyuan, Shanxi, People's Republic of China.
Li-Hui ZhangDepartment of Cardiology, Shanxi Academy of Medical Sciences and Shanxi Dayi Hospital, Shanxi Medical University, Taiyuan, Shanxi, People's Republic of China.
Feng BaiDepartment of Physiology, Shanxi Medical University, Taiyuan, Shanxi, People's Republic of China.
Ning-Ping WangDepartment of Basic Biomedical Sciences, Mercer University School of Medicine, Savannah, GA, USA.
Ron E GarnerDepartment of Basic Biomedical Sciences, Mercer University School of Medicine, Savannah, GA, USA.
Robert J McKallipDivision of Basic Biomedical Sciences, Mercer University School of Medicine, Macon, GA, USA.
Zhi-Qing ZhaoDepartment of Physiology, Shanxi Medical University, Taiyuan, Shanxi, People's Republic of China ; Department of Basic Biomedical Sciences, Mercer University School of Medicine, Savannah, GA, USA.
Mercer University · USShanxi Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Curcumin is known to improve cardiac function by balancing degradation and synthesis of collagens after myocardial infarction. This study tested the hypothesis that inhibition of myocardial fibrosis by curcumin is associated with modulating expression of angiotensin II (Ang II) receptors and angiotensin-converting enzyme 2 (ACE2). Male Sprague Dawley rats were subjected to Ang II infusion (500 ng/kg/min) using osmotic minipumps for 2 and 4 weeks, respectively, and curcumin (150 mg/kg/day) was fed by gastric gavage during Ang II infusion. Compared to the animals with Ang II infusion, curcumin significantly decreased the mean arterial blood pressure during the course of the observation. The protein level of the Ang II type 1 (AT1) receptor was reduced, and the Ang II type 2 (AT2) receptor was up-regulated, evidenced by an increased ratio of the AT2 receptor over the AT1 receptor in the curcumin group (1.2±0.02%) vs in the Ang II group (0.7±0.03%, P<0.05). These changes were coincident with less locally expressed AT1 receptor and enhanced AT2 receptor in the intracardiac vessels and intermyocardium. Along with these modulations, curcumin significantly decreased the populations of macrophages and alpha smooth muscle actin-expressing myofibroblasts, which were accompanied by reduced expression of transforming growth factor beta 1 and phosphorylated-Smad2/3. Collagen I synthesis was inhibited, and tissue fibrosis was attenuated, as demonstrated by less extensive collagen-rich fibrosis. Furthermore, curcumin increased protein level of ACE2 and enhanced its expression in the intermyocardium relative to the Ang II group. These results suggest that curcumin could be considered as an add-on therapeutic agent in the treatment of fibrosis-derived heart failure patient who is intolerant of ACE inhibitor therapy.

Indexed as

Angiotensin-Converting Enzyme 2AnimalsBlood PressureCurcuminDisease Models, AnimalFibrosisGene Expression RegulationMaleMyocardiumPeptidyl-Dipeptidase ARatsRats, Sprague-DawleyReceptor, Angiotensin, Type 1Receptor, Angiotensin, Type 2Ace2 protein, ratAngiotensin-Converting Enzyme 2CurcuminPeptidyl-Dipeptidase AReceptor, Angiotensin, Type 1Receptor, Angiotensin, Type 2angiotensin-converting enzyme 2angiotensin II receptorscollagencurcuminmyocardial fibrosis

Identifiers

PMID26648693
PMCPMC4651552
OpenAlexW2141094734

What OpenQuestion holds

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LicenceCC BY-NC
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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.