Evidence map›Paper›PMID 21626163›Full record

ReviewHeart failure reviews2012

Diabetic cardiomyopathy: understanding the molecular and cellular basis to progress in diagnosis and treatment.

Inês Falcão-Pires, Adelino F Leite-Moreira

Abstract readReview
PubMed Publisher
In one paragraph

Review in Heart failure reviews, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 185 papers.

0numbers the graph read from it
0cells of the map it votes in
185citing papers in PubMed
13.9field-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

185 citing papers in PubMed, 362 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
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  5. The impact of diabetes on giant negative T-wave amplitude in apical hypertrophic cardiomyopathy patients.American heart journal plus : cardiology research and practice · 2026
    Article
  6. Article
  7. Review
  8. Review
  9. ALDH2 Enzyme Deficiency in Diabetic Cardiomyopathy.International journal of molecular sciences · 2025
    Review
  10. Review
  11. Article
  12. Review
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Review
  19. The impact of diabetes on tight junctions in cardiomyopathy dysfunction.Journal of diabetes and metabolic disorders · 2024
    Review
  20. Insulin-Heart Axis: Bridging Physiology to Insulin Resistance.International journal of molecular sciences · 2024
    Review

125 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 1 institution in 1 country.

Inês Falcão-PiresDepartment of Physiology and Cardiothoracic Surgery, Cardiovascular R&D Unit, University of Porto, Porto, Portugal.
Adelino F Leite-Moreira
Universidade do Porto · PT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Diabetes mellitus is an important and prevalent risk factor for congestive heart failure. Diabetic cardiomyopathy has been defined as ventricular dysfunction that occurs in diabetic patients independent of a recognized cause such as coronary artery disease or hypertension. The disease course consists of a hidden subclinical period, during which cellular structural insults and abnormalities lead initially to diastolic dysfunction, later to systolic dysfunction, and eventually to heart failure. Left ventricular hypertrophy, metabolic abnormalities, extracellular matrix changes, small vessel disease, cardiac autonomic neuropathy, insulin resistance, oxidative stress, and apoptosis are the most important contributors to diabetic cardiomyopathy onset and progression. Hyperglycemia is a major etiological factor in the development of diabetic cardiomyopathy. It increases the levels of free fatty acids and growth factors and causes abnormalities in substrate supply and utilization, calcium homeostasis, and lipid metabolism. Furthermore, it promotes excessive production and release of reactive oxygen species, which induces oxidative stress leading to abnormal gene expression, faulty signal transduction, and cardiomyocytes apoptosis. Stimulation of connective tissue growth factor, fibrosis, and the formation of advanced glycation end-products increase the stiffness of the diabetic hearts. Despite all the current information on diabetic cardiomyopathy, translational research is still scarce due to limited human myocardial tissue and most of our knowledge is extrapolated from animals. This paper aims to elucidate some of the molecular and cellular pathophysiologic mechanisms, structural changes, and therapeutic strategies that may help struggle against diabetic cardiomyopathy.

Indexed as

Diabetic CardiomyopathiesHumansHyperglycemiaInsulin ResistanceMyocytes, CardiacOxidative StressVentricular Dysfunction

Identifiers

PMID21626163
OpenAlexW2028097684

What OpenQuestion holds

Textmetadata
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.