Evidence map›Paper›PMID 30857271›Full record

ReviewInternational journal of molecular sciences2019

Molecular Mechanisms Responsible for Diastolic Dysfunction in Diabetes Mellitus Patients.

Jovana Nikolajević Starčević, Miodrag Janić, Mišo Šabovič

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed, 1 pooled it
6.0field-weighted citation impact, top 3% 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

35 citing papers in PubMed, 1 synthesis or guideline pooled it, 59 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Diabetes and cancer: therapeutic implications.Cardio-oncology (London, England) · 2026
    Review
  6. Review
  7. Article
  8. Review
  9. Review
  10. Review
  11. Article
  12. Diabetic cardiomyopathy: pathophysiology, imaging assessment and therapeutical strategies.International journal of cardiology. Cardiovascular risk and prevention · 2024
    Review
  13. Advances in the Insulin-Heart Axis: Current Therapies and Future Directions.International journal of molecular sciences · 2024
    Review
  14. Review
  15. Article
  16. Article
  17. Review
  18. Endothelial cell-specific mineralocorticoid receptor activation promotes diastolic dysfunction in diet-induced obese male mice.American journal of physiology. Regulatory, integrative and comparative physiology · 2023
    Article
  19. Effects of altered cellular ultrastructure on energy metabolism in diabetic cardiomyopathy: anPhilosophical transactions of the Royal Society of London. Series B, Biological sciences · 2022
    Article
  20. 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

3 authors at 1 institution in 1 country.

Jovana Nikolajević StarčevićDepartment of Vascular Diseases, University Medical Centre Ljubljana, Zaloška cesta 7; SI-1000 Ljubljana, Slovenia. jovana_nikolajevic@yahoo.com.
Miodrag JanićDepartment of Vascular Diseases, University Medical Centre Ljubljana, Zaloška cesta 7; SI-1000 Ljubljana, Slovenia. miodrag.janic@kclj.si.ORCID 0000-0001-7073-8922
Mišo ŠabovičDepartment of Vascular Diseases, University Medical Centre Ljubljana, Zaloška cesta 7; SI-1000 Ljubljana, Slovenia. miso.sabovic@kclj.si.
Ljubljana University Medical Centre · SI

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In diabetic patients, cardiomyopathy is an important cause of heart failure, but its pathophysiology has not been completely understood thus far. Myocardial hypertrophy and diastolic dysfunction have been considered the hallmarks of diabetic cardiomyopathy (DCM), while systolic function is affected in the latter stages of the disease. In this article we propose the potential pathophysiological mechanisms responsible for myocardial hypertrophy and increased myocardial stiffness leading to diastolic dysfunction in this specific entity. According to our model, increased myocardial stiffness results from both cellular and extracellular matrix stiffness as well as cell⁻matrix interactions. Increased intrinsic cardiomyocyte stiffness is probably the most important contributor to myocardial stiffness. It results from the impairment in cardiomyocyte cytoskeleton. Several other mechanisms, specifically affected by diabetes, seem to also be significantly involved in myocardial stiffening, i.e., impairment in the myocardial nitric oxide (NO) pathway, coronary microvascular dysfunction, increased inflammation and oxidative stress, and myocardial sodium glucose cotransporter-2 (SGLT-2)-mediated effects. Better understanding of the complex pathophysiology of DCM suggests the possible value of drugs targeting the listed mechanisms. Antidiabetic drugs, NO-stimulating agents, anti-inflammatory agents, and SGLT-2 inhibitors are emerging as potential treatment options for DCM.

Indexed as

DiastoleAnimalsDiabetic CardiomyopathiesDisease Models, AnimalHeartHeart FailureHumansInflammationMyocytes, CardiacNitric OxideOxidative StressSodium-Glucose Transporter 2Nitric OxideSodium-Glucose Transporter 2diabetesdiabetic cardiomyopathydiastolic dysfunctionheart failuremechanisms

Identifiers

PMID30857271
PMCPMC6429211
OpenAlexW2922020200

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.