Evidence map›Paper›PMID 31269778›Full record

ReviewInternational journal of molecular sciences2019

Molecular Dysfunction and Phenotypic Derangement in Diabetic Cardiomyopathy.

Isabella Evangelista, Ranuccio Nuti, Tommaso Picchioni, Francesco Dotta, Alberto Palazzuoli

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 97 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
97citing papers in PubMed, 2 pooled it
12.6field-weighted citation impact, top 1% 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

97 citing papers in PubMed, 2 syntheses or guidelines pooled it, 172 citations in OpenAlex.

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37 more citing papers are in PubMed but not listed here.

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

5 authors at 1 institution in 1 country.

Isabella EvangelistaCardiovascular Diseases Unit, Department of Internal Medicine, Le Scotte Hospital University of Siena, Viale Bracci, 53100 Siena, Italy.ORCID 0000-0002-3828-1624
Ranuccio NutiCardiovascular Diseases Unit, Department of Internal Medicine, Le Scotte Hospital University of Siena, Viale Bracci, 53100 Siena, Italy.
Tommaso PicchioniCardiovascular Diseases Unit, Department of Internal Medicine, Le Scotte Hospital University of Siena, Viale Bracci, 53100 Siena, Italy.
Francesco DottaDiabetes Unit, Department of Medicine, Surgery and Neurosciences, Le Scotte Hospital University of Siena, Viale Bracci, 53100 Siena, Italy.
Alberto PalazzuoliCardiovascular Diseases Unit, Department of Internal Medicine, Le Scotte Hospital University of Siena, Viale Bracci, 53100 Siena, Italy. palazzuoli2@unisi.it.
University of Siena · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The high incidence and poor prognosis of heart failure (HF) patients affected with diabetes (DM) is in part related to a specific cardiac remodeling currently recognized as diabetic cardiomyopathy (DCM). This cardiac frame occurs regardless of the presence of coronary artery diseases (CAD) and it can account for 15-20% of the total diabetic population. The pathogenesis of DCM remains controversial, and several molecular and cellular alterations including myocardial hypertrophy, interstitial fibrosis, oxidative stress and vascular inflammation, have been postulated. The main cardio-vascular alterations associated with hyperglycemia comprise endothelial dysfunction, adverse effects of circulating free fatty acids (FFA) and increased systemic inflammation. High glucose concentrations lead to a loss of mitochondrial networks, increased reactive oxygen species (ROS), endothelial nitric oxide synthase (eNOS) activation and a reduction in cGMP production related to protein kinase G (PKG) activity. Current mechanisms enhance the collagen deposition with subsequent increased myocardial stiffness. Several concerns regarding the exact role of DCM in HF development such as having an appearance as either dilated or as a concentric phenotype and whether diabetes could be considered a causal factor or a comorbidity in HF, remain to be clarified. In this review, we sought to explain the different DCM subtypes and the underlying pathophysiological mechanisms. Therefore, the traditional and new molecular and signal alterations and their relationship with macroscopic structural abnormalities are described.

Indexed as

AnimalsDiabetic CardiomyopathiesGene Expression RegulationGlycation End Products, AdvancedHumansHyperglycemiaInflammationMicroRNAsMyocardiumOxidative StressGlycation End Products, AdvancedMicroRNAsdiabetesdiabetic cardiomyopathyheart failuremolecular signal derangementmyocardial remodeling

Identifiers

PMID31269778
PMCPMC6651260
OpenAlexW2954531847

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.