Evidence map›Paper›PMID 29449364›Full record

ReviewCirculation research2018

Diabetic Cardiomyopathy: An Update of Mechanisms Contributing to This Clinical Entity.

Guanghong Jia, Michael A Hill, James R Sowers

Open access · bronzeAbstract readReview
In one paragraph

Review in Circulation research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1,069 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
1,069citing papers in PubMed, 1 pooled it
94.0field-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

1,069 citing papers in PubMed, 1 synthesis or guideline pooled it, 1,717 citations in OpenAlex.

  1. Pooled it
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  13. Binaphthoquinone attenuates myofibroblast transition of human ventricular cardiac fibroblastsThe Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2026
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  17. Which heart failure phenotypes benefit from GLP-1 receptor agonists?Cardiovascular diabetology. Endocrinology reports · 2026
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1,009 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

3 authors at 1 institution in 1 country.

Guanghong JiaFrom the Diabetes and Cardiovascular Research Center (G.J., J.R.S.) and Department of Medical Pharmacology and Physiology (M.A.H., J.R.S.), University of Missouri School of Medicine, Columbia; Dalton Cardiovascular Research Center, University of Missouri, Columbia (M.A.H., J.R.S.); and Research Service, Truman Memorial Veterans Hospital, Columbia, MO (G.J., J.R.S.).
Michael A HillFrom the Diabetes and Cardiovascular Research Center (G.J., J.R.S.) and Department of Medical Pharmacology and Physiology (M.A.H., J.R.S.), University of Missouri School of Medicine, Columbia; Dalton Cardiovascular Research Center, University of Missouri, Columbia (M.A.H., J.R.S.); and Research Service, Truman Memorial Veterans Hospital, Columbia, MO (G.J., J.R.S.).
James R SowersFrom the Diabetes and Cardiovascular Research Center (G.J., J.R.S.) and Department of Medical Pharmacology and Physiology (M.A.H., J.R.S.), University of Missouri School of Medicine, Columbia; Dalton Cardiovascular Research Center, University of Missouri, Columbia (M.A.H., J.R.S.); and Research Service, Truman Memorial Veterans Hospital, Columbia, MO (G.J., J.R.S.). Sowersj@health.missouri.edu Jiag@health.missouri.edu.
University of Missouri · US

Funding

Role of Cytokine-Induced Inflammation in Endothelial Dysfunction in DiabetesR01HL085119 · NHLBI · UNIVERSITY OF MISSOURI-COLUMBIA · PI HILL, MICHAEL A · 2007 to 2015
$3.1M
ANG II OPPOSES INS MEDIATED VASORELAXATION &GLU UTILZAR01HL073101 · NHLBI · UNIVERSITY OF MISSOURI-COLUMBIA · PI SOWERS, JAMES RUSSELL · 2004 to 2013
$2.7M
Ang II and Overnutrition and Insulin resistance in Cardiovascular TissueR01HL107910 · NHLBI · UNIVERSITY OF MISSOURI-COLUMBIA · PI SOWERS, JAMES RUSSELL · 2011 to 2015
$1.8M
Interactions of the RAAS and a Western Diet on Insulin Metabolic ActionsI01BX001981 · VA · HARRY S. TRUMAN MEMORIAL VA HOSPITAL · PI LASTRA, GUIDO · 2013 to 2022
–
BLRD VA I01 BX001981NHLBI NIH HHS R01 HL073101NHLBI NIH HHS R01 HL085119NHLBI NIH HHS R01 HL107910
6 · The paper itself

Abstract

Heart failure and related morbidity and mortality are increasing at an alarming rate, in large part, because of increases in aging, obesity, and diabetes mellitus. The clinical outcomes associated with heart failure are considerably worse for patients with diabetes mellitus than for those without diabetes mellitus. In people with diabetes mellitus, the presence of myocardial dysfunction in the absence of overt clinical coronary artery disease, valvular disease, and other conventional cardiovascular risk factors, such as hypertension and dyslipidemia, has led to the descriptive terminology, diabetic cardiomyopathy. The prevalence of diabetic cardiomyopathy is increasing in parallel with the increase in diabetes mellitus. Diabetic cardiomyopathy is initially characterized by myocardial fibrosis, dysfunctional remodeling, and associated diastolic dysfunction, later by systolic dysfunction, and eventually by clinical heart failure. Impaired cardiac insulin metabolic signaling, mitochondrial dysfunction, increases in oxidative stress, reduced nitric oxide bioavailability, elevations in advanced glycation end products and collagen-based cardiomyocyte and extracellular matrix stiffness, impaired mitochondrial and cardiomyocyte calcium handling, inflammation, renin-angiotensin-aldosterone system activation, cardiac autonomic neuropathy, endoplasmic reticulum stress, microvascular dysfunction, and a myriad of cardiac metabolic abnormalities have all been implicated in the development and progression of diabetic cardiomyopathy. Molecular mechanisms linked to the underlying pathophysiological changes include abnormalities in AMP-activated protein kinase, peroxisome proliferator-activated receptors, O-linked N-acetylglucosamine, protein kinase C, microRNA, and exosome pathways. The aim of this review is to provide a contemporary view of these instigators of diabetic cardiomyopathy, as well as mechanistically based strategies for the prevention and treatment of diabetic cardiomyopathy.

Indexed as

Signal TransductionAnimalsDiabetic CardiomyopathiesHumansInsulinMyocardiumInsulindiabetes mellitusheart failuremyocytes, cardiacperoxisome proliferator-activated receptorsrenin-angiotensin system

Identifiers

PMID29449364
PMCPMC5819359
OpenAlexW2792805849

What OpenQuestion 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 OpenQuestion graph.