Evidence map›Paper›PMID 35001338›Full record

ReviewHeart failure reviews2023

Mechanisms of cardiac dysfunction in diabetic cardiomyopathy: molecular abnormalities and phenotypical variants.

Francesca Romana Prandi, Isabella Evangelista, Domenico Sergi, Alberto Palazzuoli, Francesco Romeo

Abstract readReview
PubMed Publisher
In one paragraph

Review in Heart failure reviews, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed, 1 pooled it
12.3field-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

53 citing papers in PubMed, 1 synthesis or guideline pooled it, 78 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Article
  5. ALCAT1 promotes diabetic cardiomyopathy by linking myocardial tetralinoleoyl cardiolipin deficiency to lipotoxicity.Molecular therapy : the journal of the American Society of Gene Therapy · 2026
    Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. α-ALA Attenuates Cardiac Injury in Diabetic Heart Disease Mice by Modulating Inflammation and AMPKα1.Diabetes, metabolic syndrome and obesity : targets and therapy · 2025
    Article
  19. Review
  20. Role of AMP deaminase in diabetic cardiomyopathy.Molecular and cellular biochemistry · 2024
    Review
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 2 institutions in 1 country.

Francesca Romana PrandiDivision of Cardiology, University Hospital "Tor Vergata", Rome, RM, Italy. francescaromanaprandi@gmail.com.ORCID 0000-0003-1878-8871
Isabella EvangelistaCardiovascular Diseases Unit, Department of Internal Medicine, S. Maria Alle Scotte Hospital, University of Siena, Siena, Italy.
Domenico SergiDivision of Cardiology, University Hospital "Tor Vergata", Rome, RM, Italy.
Alberto PalazzuoliCardiovascular Diseases Unit, Department of Internal Medicine, S. Maria Alle Scotte Hospital, University of Siena, Siena, Italy.
Francesco RomeoDivision of Cardiology, University Hospital "Tor Vergata", Rome, RM, Italy.
University of Rome Tor Vergata · ITUniversity of Siena · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Diabetic cardiomyopathy (DCM) is a diabetes mellitus-induced pathophysiological condition characterized by cardiac structural, functional, and metabolic changes that can result in heart failure (HF), in the absence of coronary artery disease, hypertension, and valvular heart disease. Metabolic alterations such as hyperglycemia, insulin resistance, hyperinsulinemia, and increased metabolism of free fatty acids result in oxidative stress, inflammation, advanced glycation end products formation, abnormalities in calcium homeostasis, and apoptosis that are responsible for structural remodeling. Cardiac stiffness, hypertrophy, and fibrosis eventually lead to dysfunction and HF with preserved ejection fraction and/or HF with reduced ejection fraction. In this review, we analyzed in detail the cellular and molecular mechanisms and the metabolic pathways involved in the pathophysiology of DCM. Different phenotypes are observed in DCM, and it is not clear yet if the restrictive and the dilated phenotypes are distinct or represent an evolution of the same disease. Phenotypic differences can be observed between T1DM and T2DM DCM, possibly explained by the different myocardial insulin action. Further studies are needed in order to better understand the underlying mechanisms of DCM and to identify appropriate therapeutic targets and novel strategies to prevent and reverse the progression toward heart failure in diabetic patients.

Indexed as

Coronary Artery DiseaseDiabetes MellitusDiabetic CardiomyopathiesHeart FailureVentricular Dysfunction, LeftHumansMyocardiumDiabetes mellitusDiabetic cardiomyopathyHeart failureRestrictive phenotype

Identifiers

PMID35001338
OpenAlexW4205128452

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.