Evidence map›Paper›PMID 25629059›Full record

ArticleJournal of diabetes research2015

An altered pattern of myocardial histopathological and molecular changes underlies the different characteristics of type-1 and type-2 diabetic cardiac dysfunction.

Tamás Radovits, Sevil Korkmaz, Csaba Mátyás, Attila Oláh, Balázs Tamás Németh, Szabolcs Páli, Kristóf Hirschberg, Alina Zubarevich, Patricia Neh Gwanmesia, Shiliang Li and 4 more

Open access · goldAbstract read
In one paragraph

Article in Journal of diabetes research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
3.2field-weighted citation impact, top 8% 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

18 citing papers in PubMed, 29 citations in OpenAlex.

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  16. Diastolic dysfunction in prediabetic male rats: Role of mitochondrial oxidative stress.American journal of physiology. Heart and circulatory physiology · 2016
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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

14 authors at 2 institutions in 2 countries.

Tamás RadovitsDepartment of Cardiac Surgery, University of Heidelberg, INF 326 OG 2, 69120 Heidelberg, Germany ; Heart and Vascular Center, Semmelweis University, Városmajor u. 68, 1122 Budapest, Hungary.
Sevil KorkmazDepartment of Cardiac Surgery, University of Heidelberg, INF 326 OG 2, 69120 Heidelberg, Germany.
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.
Balázs Tamás NémethHeart and Vascular Center, Semmelweis University, Városmajor u. 68, 1122 Budapest, Hungary.ORCID 0000-0001-7202-8107
Szabolcs PáliDepartment of Cardiac Surgery, University of Heidelberg, INF 326 OG 2, 69120 Heidelberg, Germany ; Heart and Vascular Center, Semmelweis University, Városmajor u. 68, 1122 Budapest, Hungary.
Kristóf HirschbergDepartment of Cardiac Surgery, University of Heidelberg, INF 326 OG 2, 69120 Heidelberg, Germany.ORCID 0000-0003-3392-6021
Alina ZubarevichDepartment of Cardiac Surgery, University of Heidelberg, INF 326 OG 2, 69120 Heidelberg, Germany.
Patricia Neh GwanmesiaDepartment of Cardiac Surgery, University of Heidelberg, INF 326 OG 2, 69120 Heidelberg, Germany.
Shiliang LiDepartment of Cardiac Surgery, University of Heidelberg, INF 326 OG 2, 69120 Heidelberg, Germany.
Sivakkanan LoganathanDepartment of Cardiac Surgery, University of Heidelberg, INF 326 OG 2, 69120 Heidelberg, Germany.
Enikő BarnuczDepartment of Cardiac Surgery, University of Heidelberg, INF 326 OG 2, 69120 Heidelberg, Germany ; Heart and Vascular Center, Semmelweis University, Városmajor u. 68, 1122 Budapest, Hungary.
Béla MerkelyHeart and Vascular Center, Semmelweis University, Városmajor u. 68, 1122 Budapest, Hungary.
Gábor SzabóDepartment of Cardiac Surgery, University of Heidelberg, INF 326 OG 2, 69120 Heidelberg, Germany.
Heidelberg University · DESemmelweis University · HU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Increasing evidence suggests that both types of diabetes mellitus (DM) lead to cardiac structural and functional changes. In this study we investigated and compared functional characteristics and underlying subcellular pathological features in rat models of type-1 and type-2 diabetic cardiomyopathy. Type-1 DM was induced by streptozotocin. For type-2 DM, Zucker Diabetic Fatty (ZDF) rats were used. Left ventricular pressure-volume analysis was performed to assess cardiac function. Myocardial nitrotyrosine immunohistochemistry, TUNEL assay, hematoxylin-eosin, and Masson's trichrome staining were performed. mRNA and protein expression were quantified by qRT-PCR and Western blot. Marked systolic dysfunction in type-1 DM was associated with severe nitrooxidative stress, apoptosis, and fibrosis. These pathological features were less pronounced or absent, while cardiomyocyte hypertrophy was comparable in type-2 DM, which was associated with unaltered systolic function and increased diastolic stiffness. mRNA-expression of hypertrophy markers c-fos, c-jun, and β-MHC, as well as pro-apoptotic caspase-12, was elevated in type-1, while it remained unaltered or only slightly increased in type-2 DM. Expression of the profibrotic TGF-β 1 was upregulated in type-1 and showed a decrease in type-2 DM. We compared type-1 and type-2 diabetic cardiomyopathy in standard rat models and described an altered pattern of key pathophysiological features in the diabetic heart and corresponding functional consequences.

Indexed as

AnimalsApoptosisDiabetes ComplicationsDiabetes Mellitus, ExperimentalDiabetes Mellitus, Type 1Diabetes Mellitus, Type 2FibrosisGene Expression RegulationHeartHeart DiseasesHemodynamicsImmunohistochemistryIn Situ Nick-End LabelingMaleMyocardiumOxidative Stress3-nitrotyrosineRNA, MessengerTransforming Growth Factor beta1Tyrosine

Identifiers

PMID25629059
PMCPMC4300149
OpenAlexW2080939349

What OpenQuestion holds

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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.