Evidence map›Paper›PMID 27521417›Full record

ArticleAmerican journal of physiology. Heart and circulatory physiology2016

Diastolic dysfunction in prediabetic male rats: Role of mitochondrial oxidative stress.

Gábor Koncsos, Zoltán V Varga, Tamás Baranyai, Kerstin Boengler, Susanne Rohrbach, Ling Li, Klaus-Dieter Schlüter, Rolf Schreckenberg, Tamás Radovits, Attila Oláh and 19 more

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In one paragraph

Article in American journal of physiology. Heart and circulatory physiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.

0numbers the graph read from it
0cells of the map it votes in
55citing papers in PubMed
6.2field-weighted citation impact, top 3% 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

55 citing papers in PubMed, 97 citations in OpenAlex.

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  7. Mechanistic insight into the role of cardiac-enriched microRNAs in diabetic heart injury.American journal of physiology. Heart and circulatory physiology · 2025
    Review
  8. Article
  9. Role of AMP deaminase in diabetic cardiomyopathy.Molecular and cellular biochemistry · 2024
    Review
  10. Review
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  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Lipid Droplet-a New Target in Ischemic Heart Disease.Journal of cardiovascular translational research · 2022
    Review
  18. The Role of Mitochondrial Abnormalities in Diabetic Cardiomyopathy.International journal of molecular sciences · 2022
    Review
  19. Guidelines on models of diabetic heart disease.American journal of physiology. Heart and circulatory physiology · 2022
    Review
  20. CaPflugers Archiv : European journal of physiology · 2022
    Review
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

29 authors at 5 institutions in 4 countries.

Gábor KoncsosDepartment of Pharmacology and Pharmacotherapy, Faculty of Medicine, Semmelweis University, Budapest, Hungary.
Zoltán V VargaDepartment of Pharmacology and Pharmacotherapy, Faculty of Medicine, Semmelweis University, Budapest, Hungary; Laboratory of Cardiovascular Physiology and Tissue Injury, National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health, Bethesda, Maryland.
Tamás BaranyaiDepartment of Pharmacology and Pharmacotherapy, Faculty of Medicine, Semmelweis University, Budapest, Hungary.ORCID 0000-0002-9378-8938
Kerstin BoenglerInstitute of Physiology, Faculty of Medicine, Justus-Liebig University, Giessen, Germany.
Susanne RohrbachInstitute of Physiology, Faculty of Medicine, Justus-Liebig University, Giessen, Germany.
Ling LiInstitute of Physiology, Faculty of Medicine, Justus-Liebig University, Giessen, Germany.
Klaus-Dieter SchlüterInstitute of Physiology, Faculty of Medicine, Justus-Liebig University, Giessen, Germany.
Rolf SchreckenbergInstitute of Physiology, Faculty of Medicine, Justus-Liebig University, Giessen, Germany.
Tamás RadovitsHeart and Vascular Center, Semmelweis University, Budapest, Hungary.
Attila OláhHeart and Vascular Center, Semmelweis University, Budapest, Hungary.
Csaba MátyásHeart and Vascular Center, Semmelweis University, Budapest, Hungary.
Árpád LuxHeart and Vascular Center, Semmelweis University, Budapest, Hungary.
Mahmoud Al-KhrasaniDepartment of Pharmacology and Pharmacotherapy, Faculty of Medicine, Semmelweis University, Budapest, Hungary.
Tímea KomlódiDepartment of Medical Biochemistry, Faculty of Medicine, Semmelweis University, Budapest, Hungary.
Nóra BukoszaInstitute of Pathophysiology, Faculty of Medicine, Semmelweis University, Budapest, Hungary.
Domokos MáthéDepartment of Biophysics and Radiation Biology, Faculty of Medicine, Semmelweis University, Budapest, Hungary; CROmed Translational Research Centers, Budapest, Hungary.
László Deres1st Department of Internal Medicine, Faculty of Medicine, University of Pécs, Pécs, Hungary.
Monika BartekováInstitute of Physiology, Faculty of Medicine, Comenius University in Bratislava, Slovakia; Institute for Heart Research, Slovak Academy of Sciences, Bratislava, Slovakia.
Tomáš RajtíkDepartment of Pharmacology and Toxicology, Faculty of Pharmacy, Comenius University in Bratislava, Slovakia.
Adriana AdameováDepartment of Pharmacology and Toxicology, Faculty of Pharmacy, Comenius University in Bratislava, Slovakia.
Krisztián SzigetiDepartment of Biophysics and Radiation Biology, Faculty of Medicine, Semmelweis University, Budapest, Hungary.
Péter HamarInstitute of Pathophysiology, Faculty of Medicine, Semmelweis University, Budapest, Hungary.ORCID 0000-0002-1095-3564
Zsuzsanna HelyesDepartment of Pharmacology and Pharmacotherapy, Faculty of Medicine and Szentágothai Research Centre & MTA-PTE NAP B Chronic Pain Research Group, University of Pécs, Pécs, Hungary; and.
László TretterDepartment of Medical Biochemistry, Faculty of Medicine, Semmelweis University, Budapest, Hungary.
Pál PacherDepartment of Pharmacology and Pharmacotherapy, Faculty of Medicine, Semmelweis University, Budapest, Hungary; Laboratory of Cardiovascular Physiology and Tissue Injury, National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health, Bethesda, Maryland.
Béla MerkelyHeart and Vascular Center, Semmelweis University, Budapest, Hungary.
Zoltán GiriczDepartment of Pharmacology and Pharmacotherapy, Faculty of Medicine, Semmelweis University, Budapest, Hungary; giricz.zoltan@med.semmelweis-univ.hu.ORCID 0000-0003-2036-8665
Rainer SchulzInstitute of Physiology, Faculty of Medicine, Justus-Liebig University, Giessen, Germany.
Péter FerdinandyDepartment of Pharmacology and Pharmacotherapy, Faculty of Medicine, Semmelweis University, Budapest, Hungary.
Semmelweis University · HUJustus-Liebig-Universität Gießen · DEComenius University Bratislava · SKUniversity of Pecs · HUSlovak Academy of Sciences · SK

Funding

Mechanism of oxidative/nitrosative stress and inflammation-induced tissue injuryZIAAA000375 · NIAAA · NATIONAL INSTITUTE ON ALCOHOL ABUSE AND ALCOHOLISM · PI PACHER, PAL · 2009 to 2025
$27.8M
6 · The paper itself

Abstract

Although incidence and prevalence of prediabetes are increasing, little is known about its cardiac effects. Therefore, our aim was to investigate the effect of prediabetes on cardiac function and to characterize parameters and pathways associated with deteriorated cardiac performance. Long-Evans rats were fed with either control or high-fat chow for 21 wk and treated with a single low dose (20 mg/kg) of streptozotocin at week 4 High-fat and streptozotocin treatment induced prediabetes as characterized by slightly elevated fasting blood glucose, impaired glucose and insulin tolerance, increased visceral adipose tissue and plasma leptin levels, as well as sensory neuropathy. In prediabetic animals, a mild diastolic dysfunction was observed, the number of myocardial lipid droplets increased, and left ventricular mass and wall thickness were elevated; however, no molecular sign of fibrosis or cardiac hypertrophy was shown. In prediabetes, production of reactive oxygen species was elevated in subsarcolemmal mitochondria. Expression of mitofusin-2 was increased, while the phosphorylation of phospholamban and expression of Bcl-2/adenovirus E1B 19-kDa protein-interacting protein 3 (BNIP3, a marker of mitophagy) decreased. However, expression of other markers of cardiac auto- and mitophagy, mitochondrial dynamics, inflammation, heat shock proteins, Ca

Indexed as

Oxidative StressAdipokinesAdipose TissueAnimalsApoptosisAutophagyBody CompositionCalcium-Binding ProteinsCalcium-Calmodulin-Dependent Protein Kinase Type 2CardiomegalyDiabetes Mellitus, ExperimentalDiabetic NeuropathiesDiastoleDiet, High-FatEchocardiographyGTP PhosphohydrolasesAdipokinesBNIP3 protein, ratCalcium-Binding ProteinsCalcium-Calmodulin-Dependent Protein Kinase Type 2GTP PhosphohydrolasesHeat-Shock ProteinsMembrane ProteinsMfn2 protein, ratMitochondrial ProteinsmTOR protein, ratPhospholambanReactive Oxygen SpeciesTOR Serine-Threonine Kinasesdiabetic cardiomyopathyhigh-fat dietobesityreactive oxygen speciestype 2 diabetes

Identifiers

PMID27521417
PMCPMC5114470
OpenAlexW2516905651

What OpenQuestion holds

Textmetadata
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.