Evidence map›Paper›PMID 28781721›Full record

ArticleOxidative medicine and cellular longevity2017

The Effects of Diabetes Induction on the Rat Heart: Differences in Oxidative Stress, Inflammatory Cells, and Fibrosis between Subendocardial and Interstitial Myocardial Areas.

Maria C Guido, Alyne F Marques, Elaine R Tavares, Marcelo D Tavares de Melo, Vera M C Salemi, Raul C Maranhão

Open access · hybridAbstract read
In one paragraph

Article in Oxidative medicine and cellular longevity, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
2.3field-weighted citation impact, top 10% 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

13 citing papers in PubMed, 27 citations in OpenAlex.

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  3. Gaseous signal molecule SOThe Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2022
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  9. [Changes of two-pore K+ channel TASK-1 in diabetic myocardial injury in rats].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2018
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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

6 authors at 1 institution in 1 country.

Maria C GuidoLaboratory of Metabolism and Lipids, Heart Institute (InCor) of the Medical School of the University of São Paulo, São Paulo, SP, Brazil.
Alyne F MarquesLaboratory of Metabolism and Lipids, Heart Institute (InCor) of the Medical School of the University of São Paulo, São Paulo, SP, Brazil.
Elaine R TavaresLaboratory of Metabolism and Lipids, Heart Institute (InCor) of the Medical School of the University of São Paulo, São Paulo, SP, Brazil.
Marcelo D Tavares de MeloHeart Failure Unit and Clinical Cardiology Division, Heart Institute (InCor) of the Medical School of the University of São Paulo, São Paulo, SP, Brazil.
Vera M C SalemiHeart Failure Unit and Clinical Cardiology Division, Heart Institute (InCor) of the Medical School of the University of São Paulo, São Paulo, SP, Brazil.
Raul C MaranhãoLaboratory of Metabolism and Lipids, Heart Institute (InCor) of the Medical School of the University of São Paulo, São Paulo, SP, Brazil.ORCID 0000-0003-1520-4914
Universidade de São Paulo · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Diabetic cardiomyopathy (DCM) is characterized by cardiac remodeling and impaired diastolic function that may lead to heart failure. The aim of this study was to evaluate oxidative stress, inflammatory cells, and fibrosis in both subendocardial (SEN) and interstitial (INT) areas of the myocardium. Male Wistar rats were allocated to 2 groups of 9 animals, a control (CT) group and streptozotocin-induced diabetes (DM). After 8 weeks, echocardiography morphometry, protein expression, and confocal microscopy in SEN and INT areas of the left ventricle (LV) were performed. The echocardiographic analysis showed that diabetes induction leads to cardiac dilation, hypertrophy, and LV diastolic dysfunction. As compared to CT, the induction of diabetes increased inflammatory cells and fibrosis in both SEN and INT areas of DM myocardium and increased ROS generation only in SEN. Comparing the SEN and INT areas in the DM group, inflammatory cells and fibrosis in SEN were greater than in INT. In conclusion, diabetic myocardium SEN area, wherein oxidative stress was more pronounced, is more susceptible to cardiac dysfunction than INT area. This finding can be important for the understanding of the heart remodeling process occurring in DCM and perhaps to engender targeted therapies to attenuate or revert DCM-related diastolic dysfunction.

Indexed as

AnimalsBlotting, WesternDiabetes MellitusDiabetes Mellitus, ExperimentalDiabetic CardiomyopathiesEchocardiographyHeartMaleMyocardiumOxidative StressRatsRats, WistarReactive Oxygen SpeciesVentricular Dysfunction, LeftReactive Oxygen Species

Identifiers

PMID28781721
PMCPMC5525092
OpenAlexW2735115050

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.