Evidence map›Paper›PMID 32437308›Full record

ReviewCirculation research2020

Basic Mechanisms of Diabetic Heart Disease.

Rebecca H Ritchie, E Dale Abel

Open access · bronzeAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Circulation research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 395 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
395citing papers in PubMed, 2 pooled it
42.9field-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

395 citing papers in PubMed, 2 syntheses or guidelines pooled it, 673 citations in OpenAlex.

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  17. snRNA-seq identifies Fmo2npj metabolic health and disease · 2026
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335 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

2 authors at 2 institutions in 2 countries.

Rebecca H RitchieFrom Drug Discovery Biology, Monash Institute of Pharmaceutical Sciences, Monash University, Parkville Campus, Victoria, Australia (R.H.R.).
E Dale AbelDivision of Endocrinology and Metabolism (E.D.A.), University of Iowa Carver College of Medicine, Iowa City.
Monash University · AUUniversity of Iowa · US

Funding

Insulin resistance and cardiac dysfunction in obesityR01HL073167 · UNIVERSITY OF UTAH · 2003 to 2005
$1.3M
Insulin Signaling and the Heart in DiabetesR01HL070070 · UNIVERSITY OF UTAH · 2004 to 2005
$774k
Targeting Antioxidant Therapy to Cardiac MitochondriaR21DK073590 · UNIVERSITY OF UTAH · 2005 to 2005
$187k
NHLBI NIH HHS R01 HL070070NHLBI NIH HHS R01 HL073167NHLBI NIH HHS R01 HL108379NHLBI NIH HHS R01 HL112413NHLBI NIH HHS R01 HL127764NHLBI NIH HHS R33 HL141783NHLBI NIH HHS R61 HL141783NHLBI NIH HHS U01 HL087947NIDDK NIH HHS R01 DK092065NIDDK NIH HHS R21 DK073590
6 · The paper itself

Abstract

Diabetes mellitus predisposes affected individuals to a significant spectrum of cardiovascular complications, one of the most debilitating in terms of prognosis is heart failure. Indeed, the increasing global prevalence of diabetes mellitus and an aging population has given rise to an epidemic of diabetes mellitus-induced heart failure. Despite the significant research attention this phenomenon, termed diabetic cardiomyopathy, has received over several decades, understanding of the full spectrum of potential contributing mechanisms, and their relative contribution to this heart failure phenotype in the specific context of diabetes mellitus, has not yet been fully resolved. Key recent preclinical discoveries that comprise the current state-of-the-art understanding of the basic mechanisms of the complex phenotype, that is, the diabetic heart, form the basis of this review. Abnormalities in each of cardiac metabolism, physiological and pathophysiological signaling, and the mitochondrial compartment, in addition to oxidative stress, inflammation, myocardial cell death pathways, and neurohumoral mechanisms, are addressed. Further, the interactions between each of these contributing mechanisms and how they align to the functional, morphological, and structural impairments that characterize the diabetic heart are considered in light of the clinical context: from the disease burden, its current management in the clinic, and where the knowledge gaps remain. The need for continued interrogation of these mechanisms (both known and those yet to be identified) is essential to not only decipher the how and why of diabetes mellitus-induced heart failure but also to facilitate improved inroads into the clinical management of this pervasive clinical challenge.

Indexed as

AnimalsDiabetic CardiomyopathiesHeartHumansMyocardiumdiabetes mellitusdiabetic cardiomyopathyfibrosisheart diseasesheart failureoxidative stressventricular remodelling

Identifiers

PMID32437308
PMCPMC7251974
OpenAlexW3026907472

What Socratic holds

Textmetadata
LicenceTDM
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 Socratic graph.