Evidence map›Paper›PMID 23147391›Full record

ReviewLife sciences2013

Molecular and metabolic mechanisms of cardiac dysfunction in diabetes.

Chirag H Mandavia, Annayya R Aroor, Vincent G Demarco, James R Sowers

Open access · greenAbstract readReview
In one paragraph

Review in Life sciences, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 95 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
95citing papers in PubMed, 1 pooled it
12.1field-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

95 citing papers in PubMed, 1 synthesis or guideline pooled it, 193 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Article
  4. The heart of diabetes: unraveling metabolic drivers of cardiomyopathy.Cardiovascular diabetology. Endocrinology reports · 2025
    Review
  5. Review
  6. Review
  7. Downregulation ofCurrent diabetes reviews · 2025
    Article
  8. Review
  9. Article
  10. Insulin-Heart Axis: Bridging Physiology to Insulin Resistance.International journal of molecular sciences · 2024
    Review
  11. Article
  12. Creatine Kinase Equilibration and ΔGInternational journal of molecular sciences · 2023
    Article
  13. Article
  14. Article
  15. Review
  16. Energy substrate metabolism and oxidative stress in metabolic cardiomyopathy.Journal of molecular medicine (Berlin, Germany) · 2022
    Review
  17. Review
  18. Article
  19. Review
  20. Article

35 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

4 authors at 2 institutions in 1 country.

Chirag H MandaviaUniversity of Missouri School of Medicine, Department of Internal Medicine, Columbia, MO, USA.
Annayya R Aroor
Vincent G Demarco
James R Sowers
University of Missouri · USHarry S. Truman Memorial Veterans' Hospital · US

Funding

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
–
NHLBI NIH HHS R01 HL073101NHLBI NIH HHS R01 HL107910NHLBI NIH HHS R01 HL107910-01NHLBI NIH HHS R01 HL73101-01A
6 · The paper itself

Abstract

Diabetes mellitus type 2 (T2DM) is a widespread chronic medical condition with prevalence bordering on the verge of an epidemic. It is of great concern that cardiovascular disease is more common in patients with diabetes than the non-diabetic population. While hypertensive and ischemic heart disease is more common in diabetic patients, there is another type of heart disease in diabetes that is not associated with hypertension or coronary artery disease. This muscle functional disorder is termed "diabetic cardiomyopathy". Diastolic dysfunction characterized by impaired diastolic relaxation time and reduced contractility precedes systolic dysfunction and is the main pathogenic hallmark of this condition. Even though the pathogenesis of "diabetic cardiomyopathy" is still controversial, impaired cardiac insulin sensitivity and metabolic overload are emerging as major molecular and metabolic mechanisms for cardiac dysfunction. Systemic insulin resistance, hyperinsulinemia, dysregulation of adipokine secretion, increases in circulating levels of inflammatory mediators, aberrant activation of renin angiotensin aldosterone system (RAAS), and increased oxidative stress contribute dysregulated insulin and metabolic signaling in the heart and development of diastolic dysfunction. In addition, maladaptive calcium homeostasis and endothelial cell dysregulation endoplasmic reticular stress play a potential role in cardiomyocyte fibrosis/diastolic dysfunction. In this review, we will focus on emerging molecular and metabolic pathways underlying cardiac dysfunction in diabetes. Elucidation of these mechanisms should provide a better understanding of the various cardiac abnormalities associated with diastolic dysfunction and its progression to systolic dysfunction and heart failure.

Indexed as

Cardio-Renal SyndromeDiabetes Mellitus, Type 2Diabetic CardiomyopathiesHumansOxidative StressSignal Transduction

Identifiers

PMID23147391
PMCPMC3594135
OpenAlexW1999330035

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.