Evidence map›Paper›PMID 27853261›Full record

ArticleScientific reports2016

Cinaciguat prevents the development of pathologic hypertrophy in a rat model of left ventricular pressure overload.

Balázs Tamás Németh, Csaba Mátyás, Attila Oláh, Árpád Lux, László Hidi, Mihály Ruppert, Dalma Kellermayer, Gábor Kökény, Gábor Szabó, Béla Merkely and 1 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

12 citing papers in PubMed, 25 citations in OpenAlex.

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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

11 authors at 2 institutions in 2 countries.

Balázs Tamás NémethHeart and Vascular Center, Semmelweis University, Városmajor u. 68., 1122 Budapest, Hungary.
Csaba MátyásHeart and Vascular Center, Semmelweis University, Városmajor u. 68., 1122 Budapest, Hungary.
Attila OláhHeart and Vascular Center, Semmelweis University, Városmajor u. 68., 1122 Budapest, Hungary.
Árpád LuxHeart and Vascular Center, Semmelweis University, Városmajor u. 68., 1122 Budapest, Hungary.
László HidiHeart and Vascular Center, Semmelweis University, Városmajor u. 68., 1122 Budapest, Hungary.
Mihály RuppertHeart and Vascular Center, Semmelweis University, Városmajor u. 68., 1122 Budapest, Hungary.
Dalma KellermayerHeart and Vascular Center, Semmelweis University, Városmajor u. 68., 1122 Budapest, Hungary.
Gábor KökényInstitute of Pathophysiology, Semmelweis University, Nagyvárad tér 4., 1089 Budapest, Hungary.
Gábor SzabóDepartment of Cardiac Surgery, University of Heidelberg, Im Neuenheimer Feld 110., 69210 Heidelberg, Germany.
Béla MerkelyHeart and Vascular Center, Semmelweis University, Városmajor u. 68., 1122 Budapest, Hungary.
Tamás RadovitsHeart and Vascular Center, Semmelweis University, Városmajor u. 68., 1122 Budapest, Hungary.
Semmelweis University · HUHeidelberg University · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pathologic myocardial hypertrophy develops when the heart is chronically pressure-overloaded. Elevated intracellular cGMP-levels have been reported to prevent the development of pathologic myocardial hypertrophy, therefore we investigated the effects of chronic activation of the cGMP producing enzyme, soluble guanylate cyclase by Cinaciguat in a rat model of pressure overload-induced cardiac hypertrophy. Abdominal aortic banding (AAB) was used to evoke pressure overload-induced cardiac hypertrophy in male Wistar rats. Sham operated animals served as controls. Experimental and control groups were treated with 10 mg/kg/day Cinaciguat (Cin) or placebo (Co) p.o. for six weeks, respectively. Pathologic myocardial hypertrophy was present in the AABCo group following 6 weeks of pressure overload of the heart, evidenced by increased relative heart weight, average cardiomyocyte diameter, collagen content and apoptosis. Cinaciguat did not significantly alter blood pressure, but effectively attenuated all features of pathologic myocardial hypertrophy, and normalized functional changes, such as the increase in contractility following AAB. Our results demonstrate that chronic enhancement of cGMP signalling by pharmacological activation of sGC might be a novel therapeutic approach in the prevention of pathologic myocardial hypertrophy.

Indexed as

AnimalsApoptosisBenzoatesBlood PressureCyclic GMPHypertrophy, Left VentricularMaleMyocardiumRatsRats, WistarSecond Messenger SystemsBAY 58-2667BenzoatesCyclic GMP

Identifiers

PMID27853261
PMCPMC5112572
OpenAlexW2551768950

What OpenQuestion holds

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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.