Evidence map›Paper›PMID 21927577›Full record

ArticleInternational journal of biological sciences2011

Cardioprotective effects of telmisartan against heart failure in rats induced by experimental autoimmune myocarditis through the modulation of angiotensin-converting enzyme-2/angiotensin 1-7/mas receptor axis.

Vijayakumar Sukumaran, Punniyakoti T Veeraveedu, Narasimman Gurusamy, Ken'ichi Yamaguchi, Arun Prasath Lakshmanan, Meilei Ma, Kenji Suzuki, Makoto Kodama, Kenichi Watanabe

Open access · goldAbstract read
In one paragraph

Article in International journal of biological sciences, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
60citing papers in PubMed, 2 pooled it
3.7field-weighted citation impact, top 6% 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

60 citing papers in PubMed, 2 syntheses or guidelines pooled it, 122 citations in OpenAlex.

  1. Pooled it
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  12. Sex Difference in MasR Expression and Functions in the Renal System.Journal of the renin-angiotensin-aldosterone system : JRAAS · 2022
    Review
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  16. Do Changes inInternational journal of molecular sciences · 2021
    Review
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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

9 authors at 3 institutions in 2 countries.

Vijayakumar SukumaranDepartment of Clinical Pharmacology, Faculty of Pharmaceutical Sciences, Niigata University of Pharmacy and Applied Life Sciences, Niigata, Japan. svkumar1979@yahoo.com
Punniyakoti T Veeraveedu
Narasimman Gurusamy
Ken'ichi Yamaguchi
Arun Prasath Lakshmanan
Meilei Ma
Kenji Suzuki
Makoto Kodama
Kenichi Watanabe
Niigata University of Pharmacy and Applied Life Sciences · JPHarvard University Press · USOsaka University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Angiotensin-converting enzyme-2 (ACE-2) is a homolog of ACE that preferentially forms angiotensin-(ANG)-1-7 from angiotensin II (ANG II). We investigated the cardioprotective effects of telmisartan, a well-known angiotensin receptor blockers (ARBs) against experimental autoimmune myocarditis (EAM). EAM was induced in Lewis rats by immunization with porcine cardiac myosin. The rats were divided into two groups and treated with telmisartan (10 mg/kg/day) or vehicle for 21 days. Myocardial functional parameters were significantly improved by treatment with telmisartan compared with vehicle-treated rats. Telmisartan lowered myocardial protein expressions of NADPH oxidase subunits 3-nitrotyrosine, p47phox, p67 phox, Nox-4 and superoxide production significantly than vehicle-treated rats. In contrast myocardial protein levels of ACE-2, ANG 1-7 mas receptor were upregulated in the telmisartan treated group compared with those of vehicle-treated rats. The myocardial protein expression levels of tumor necrosis factor receptor (TNFR)-associated factor (TRAF)-2, C/EBP homologous protein (CHOP) and glucose-regulated protein (GRP) 78 were decreased in the telmisartan treated rats compared with those of vehicle-treated rats. In addition, telmisartan treatment significantly decreased the protein expression levels of phospho-p38 mitogen-activated protein kinase (MAPK), phospho-JNK, phospho-ERK and phospho (MAPK) activated protein kinase-2 than with those of vehicle-treated rats. Moreover, telmisartan significantly decreased the production of proinflammatory cytokines, myocardial apoptotic markers and caspase-3 positive cells compared with those of vehicle-treated rats. Therefore, we suggest that telmisartan was beneficial protection against heart failure in rats, at least in part by suppressing inflammation, oxidative stress, ER stress as well as signaling pathways through the modulation of ACE2/ANG1-7/Mas receptor axis.

Indexed as

Angiotensin-Converting Enzyme 2Angiotensin IAngiotensin II Type 1 Receptor BlockersAnimalsApoptosisBenzimidazolesBenzoatesBiomarkersCytokinesDisease Models, AnimalEndoplasmic ReticulumHeart FailureMaleMitogen-Activated Protein KinasesMyocarditisNADPH OxidasesAce2 protein, ratAngiotensin-Converting Enzyme 2Angiotensin Iangiotensin I (1-7)Angiotensin II Type 1 Receptor BlockersBenzimidazolesBenzoatesBiomarkersCytokinesMitogen-Activated Protein KinasesNADPH OxidasesPeptide FragmentsPeptidyl-Dipeptidase AProtective AgentsProtein SubunitsSuperoxidesTelmisartanendoplasmic reticulum stressExperimental autoimmune myocarditisinflammationoxidative stresssignaling pathwaystelmisartan

Identifiers

PMID21927577
PMCPMC3174385
OpenAlexW2118638261

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.