Evidence map›Paper›PMID 34829647›Full record

ArticleAntioxidants (Basel, Switzerland)2021

Long-Term PDE-5A Inhibition Improves Myofilament Function in Left and Right Ventricular Cardiomyocytes through Partially Different Mechanisms in Diabetic Rat Hearts.

Beáta Bódi, Árpád Kovács, Hajnalka Gulyás, Lilla Mártha, Attila Tóth, Csaba Mátyás, Bálint András Barta, Attila Oláh, Béla Merkely, Tamás Radovits and 1 more

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

Article in Antioxidants (Basel, Switzerland), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.3field-weighted citation impact, top 38% 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

2 citing papers in PubMed, 3 citations in OpenAlex.

  1. Article
  2. Article
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 1 country.

Beáta BódiDivision of Clinical Physiology, Department of Cardiology, Faculty of Medicine, University of Debrecen, 4032 Debrecen, Hungary.
Árpád KovácsDivision of Clinical Physiology, Department of Cardiology, Faculty of Medicine, University of Debrecen, 4032 Debrecen, Hungary.
Hajnalka GulyásDivision of Clinical Physiology, Department of Cardiology, Faculty of Medicine, University of Debrecen, 4032 Debrecen, Hungary.
Lilla MárthaDivision of Clinical Physiology, Department of Cardiology, Faculty of Medicine, University of Debrecen, 4032 Debrecen, Hungary.
Attila TóthDivision of Clinical Physiology, Department of Cardiology, Faculty of Medicine, University of Debrecen, 4032 Debrecen, Hungary.ORCID 0000-0001-6503-3653
Csaba MátyásHeart and Vascular Center, Semmelweis University, 1122 Budapest, Hungary.ORCID 0000-0001-6095-7611
Bálint András BartaHeart and Vascular Center, Semmelweis University, 1122 Budapest, Hungary.
Attila OláhHeart and Vascular Center, Semmelweis University, 1122 Budapest, Hungary.
Béla MerkelyHeart and Vascular Center, Semmelweis University, 1122 Budapest, Hungary.
Tamás RadovitsHeart and Vascular Center, Semmelweis University, 1122 Budapest, Hungary.
Zoltán PappDivision of Clinical Physiology, Department of Cardiology, Faculty of Medicine, University of Debrecen, 4032 Debrecen, Hungary.ORCID 0000-0002-4675-1542
University of Debrecen · HUSemmelweis University · HU

Funding

European Union and the European Regional Development Fund GINOP-2.3.2-15-2016-00048Ministry for Innovation and Technology in Hungary, within the framework of the Therapeutic Development and Bioimaging thematic programmes of the Semmelweis University Thematic Excellence Programme (2020-4.1.1.-TKP2020)National Research, Development and Innovation Fund of Hungary K 132623National Research, Development and Innovation Fund of Hungary K 134939National Research, Development and Innovation Fund of Hungary, financed under the NVKP_16 funding scheme NVKP_16-1-2016-0017National Research, Development and Innovation Fund of Hungary, under the 2020-4.1.1-TKP2020 funding scheme TKP2020-IKA-04 and TKP2020-NKA-04
6 · The paper itself

Abstract

Heart failure with preserved ejection fraction (HFpEF) and right ventricular (RV) dysfunction are frequent complications of diabetic cardiomyopathy. Here we aimed to characterize RV and left ventricular (LV) remodeling and its prevention by vardenafil (a long-acting phosphodiesterase-5A (PDE-5A) inhibitor) administration in a diabetic HFpEF model. Zucker Diabetic Fatty (ZDF) and control, ZDF Lean (Lean) male rats received 10 mg/kg vardenafil (ZDF + Vard; Lean + Vard) per os, on a daily basis for a period of 25 weeks. In vitro force measurements, biochemical and histochemical assays were employed to assess cardiomyocyte function and signaling. Vardenafil treatment increased cyclic guanosine monophosphate (cGMP) levels and decreased 3-nitrotyrosine (3-NT) levels in the left and right ventricles of ZDF animals, but not in Lean animals. Cardiomyocyte passive tension (F

Indexed as

Ca2+-sensitivity of force productioncardiomyocyte passive tensiondiabetic cardiomyopathyHFpEFmyofilament protein phosphorylationphosphodiesterase-5Aright ventriclevardenafil

Identifiers

PMID34829647
PMCPMC8615283
OpenAlexW3212469751

What OpenQuestion holds

Textmetadata
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.