Evidence map›Paper›PMID 26185602›Full record

ReviewWorld journal of diabetes2015

Contractile apparatus dysfunction early in the pathophysiology of diabetic cardiomyopathy.

Mark T Waddingham, Amanda J Edgley, Hirotsugu Tsuchimochi, Darren J Kelly, Mikiyasu Shirai, James T Pearson

Open access · diamondAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in World journal of diabetes, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed, 1 pooled it
4.7field-weighted citation impact, top 4% 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

29 citing papers in PubMed, 1 synthesis or guideline pooled it, 65 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Article
  5. Review
  6. Article
  7. Review
  8. Review
  9. Review
  10. The interplay of inflammation, exosomes and CaCardiovascular diabetology · 2023
    Review
  11. Article
  12. Review
  13. Review
  14. Article
  15. Systolic Dysfunction of the Heart in Type 1 Diabetes Mellitus.Bulletin of experimental biology and medicine · 2021
    Article
  16. Article
  17. Review
  18. Article
  19. Article
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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

6 authors at 1 institution in 1 country.

Mark T WaddinghamMark T Waddingham, Amanda J Edgley, Darren J Kelly, Department of Medicine, St Vincent's Hospital, University of Melbourne, Melbourne, Victoria 3065, Australia.
Amanda J EdgleyMark T Waddingham, Amanda J Edgley, Darren J Kelly, Department of Medicine, St Vincent's Hospital, University of Melbourne, Melbourne, Victoria 3065, Australia.
Hirotsugu TsuchimochiMark T Waddingham, Amanda J Edgley, Darren J Kelly, Department of Medicine, St Vincent's Hospital, University of Melbourne, Melbourne, Victoria 3065, Australia.
Darren J KellyMark T Waddingham, Amanda J Edgley, Darren J Kelly, Department of Medicine, St Vincent's Hospital, University of Melbourne, Melbourne, Victoria 3065, Australia.
Mikiyasu ShiraiMark T Waddingham, Amanda J Edgley, Darren J Kelly, Department of Medicine, St Vincent's Hospital, University of Melbourne, Melbourne, Victoria 3065, Australia.
James T PearsonMark T Waddingham, Amanda J Edgley, Darren J Kelly, Department of Medicine, St Vincent's Hospital, University of Melbourne, Melbourne, Victoria 3065, Australia.
University of Melbourne · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Diabetes mellitus significantly increases the risk of cardiovascular disease and heart failure in patients. Independent of hypertension and coronary artery disease, diabetes is associated with a specific cardiomyopathy, known as diabetic cardiomyopathy (DCM). Four decades of research in experimental animal models and advances in clinical imaging techniques suggest that DCM is a progressive disease, beginning early after the onset of type 1 and type 2 diabetes, ahead of left ventricular remodeling and overt diastolic dysfunction. Although the molecular pathogenesis of early DCM still remains largely unclear, activation of protein kinase C appears to be central in driving the oxidative stress dependent and independent pathways in the development of contractile dysfunction. Multiple subcellular alterations to the cardiomyocyte are now being highlighted as critical events in the early changes to the rate of force development, relaxation and stability under pathophysiological stresses. These changes include perturbed calcium handling, suppressed activity of aerobic energy producing enzymes, altered transcriptional and posttranslational modification of membrane and sarcomeric cytoskeletal proteins, reduced actin-myosin cross-bridge cycling and dynamics, and changed myofilament calcium sensitivity. In this review, we will present and discuss novel aspects of the molecular pathogenesis of early DCM, with a special focus on the sarcomeric contractile apparatus.

Indexed as

DiabetesInsulin resistanceMyocardiumPrediabetesProtein kinase CRho kinaseSarcomere

Identifiers

PMID26185602
PMCPMC4499528
OpenAlexW2400905892

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.