Evidence map›Paper›PMID 34074290›Full record

ArticleCardiovascular diabetology2021

Diastolic dysfunction in a pre-clinical model of diabetes is associated with changes in the cardiac non-myocyte cellular composition.

Charles D Cohen, Miles J De Blasio, Man K S Lee, Gabriella E Farrugia, Darnel Prakoso, Crisdion Krstevski, Minh Deo, Daniel G Donner, Helen Kiriazis, Michelle C Flynn and 5 more

Open access · goldAbstract read
In one paragraph

Article in Cardiovascular diabetology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed, 1 pooled it
2.5field-weighted citation impact, top 10% 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

16 citing papers in PubMed, 1 synthesis or guideline pooled it, 22 citations in OpenAlex.

  1. Myocardial Immune Cells: The Basis of Cardiac Immunology.Journal of immunology (Baltimore, Md. : 1950) · 2023
    Pooled it
  2. Review
  3. Article
  4. Guidelines for diet-induced models of cardiometabolic syndrome.American journal of physiology. Heart and circulatory physiology · 2025
    Review
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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

15 authors at 2 institutions in 1 country.

Charles D CohenHeart Failure Pharmacology, Drug Discovery Biology, Monash Institute of Pharmaceutical Sciences, 399 Royal Parade, Parkville, VIC, 3052, Australia.
Miles J De BlasioHeart Failure Pharmacology, Drug Discovery Biology, Monash Institute of Pharmaceutical Sciences, 399 Royal Parade, Parkville, VIC, 3052, Australia.
Man K S LeeHaematopoiesis and Leukocyte Biology, Baker Heart and Diabetes Institute, Prahran, VIC, Australia.
Gabriella E FarrugiaCardiac Cellular Systems, Baker Heart and Diabetes Institute, 75 Commercial Road, Melbourne, VIC, 3004, Australia.
Darnel PrakosoHeart Failure Pharmacology, Drug Discovery Biology, Monash Institute of Pharmaceutical Sciences, 399 Royal Parade, Parkville, VIC, 3052, Australia.
Crisdion KrstevskiCardiac Cellular Systems, Baker Heart and Diabetes Institute, 75 Commercial Road, Melbourne, VIC, 3004, Australia.
Minh DeoHeart Failure Pharmacology, Drug Discovery Biology, Monash Institute of Pharmaceutical Sciences, 399 Royal Parade, Parkville, VIC, 3052, Australia.
Daniel G DonnerPreclinical Cardiology, Microsurgery & Imaging Platform, Baker Heart and Diabetes Institute, Prahran, VIC, Australia.
Helen KiriazisPreclinical Cardiology, Microsurgery & Imaging Platform, Baker Heart and Diabetes Institute, Prahran, VIC, Australia.
Michelle C FlynnHaematopoiesis and Leukocyte Biology, Baker Heart and Diabetes Institute, Prahran, VIC, Australia.
Taylah L GaynorCardiac Cellular Systems, Baker Heart and Diabetes Institute, 75 Commercial Road, Melbourne, VIC, 3004, Australia.
Andrew J MurphyHaematopoiesis and Leukocyte Biology, Baker Heart and Diabetes Institute, Prahran, VIC, Australia.
Grant R DrummondDepartment of Physiology, Microbiology and Anatomy, La Trobe University, Bundoora, VIC, Australia.
Alexander R Pinto *Cardiac Cellular Systems, Baker Heart and Diabetes Institute, 75 Commercial Road, Melbourne, VIC, 3004, Australia. alex.pinto@baker.edu.au.
Rebecca H Ritchie *Heart Failure Pharmacology, Drug Discovery Biology, Monash Institute of Pharmaceutical Sciences, 399 Royal Parade, Parkville, VIC, 3052, Australia. Rebecca.ritchie@monash.edu.ORCID 0000-0002-8610-0058
Baker Heart and Diabetes Institute · AULa Trobe University · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundDiabetes is associated with a significantly elevated risk of cardiovascular disease and its specific pathophysiology remains unclear. Recent studies have changed our understanding of cardiac cellularity, with cellular changes accompanying diabetes yet to be examined in detail. This study aims to characterise the changes in the cardiac cellular landscape in murine diabetes to identify potential cellular protagonists in the diabetic heart.

methodsDiabetes was induced in male FVB/N mice by low-dose streptozotocin and a high-fat diet for 26-weeks. Cardiac function was measured by echocardiography at endpoint. Flow cytometry was performed on cardiac ventricles as well as blood, spleen, and bone-marrow at endpoint from non-diabetic and diabetic mice. To validate flow cytometry results, immunofluorescence staining was conducted on left-ventricles of age-matched mice.

resultsMice with diabetes exhibited hyperglycaemia and impaired glucose tolerance at endpoint. Echocardiography revealed reduced E:A and e':a' ratios in diabetic mice indicating diastolic dysfunction. Systolic function was not different between the experimental groups. Detailed examination of cardiac cellularity found resident mesenchymal cells (RMCs) were elevated as a result of diabetes, due to a marked increase in cardiac fibroblasts, while smooth muscle cells were reduced in proportion. Moreover, we found increased levels of Ly6C

conclusionsMurine diabetes results in distinct changes in cardiac cellularity. These changes-in particular increased levels of fibroblasts-offer a framework for understanding how cardiac cellularity changes in diabetes. The results also point to new cellular mechanisms in this context, which may further aid in development of pharmacotherapies to allay the progression of cardiomyopathy associated with diabetes.

Indexed as

Ventricular Function, LeftAnimalsBlood GlucoseDiabetes Mellitus, ExperimentalDiabetic CardiomyopathiesDiastoleDiet, High-FatFibroblastsHematopoietic Stem CellsMaleMiceMonocytesMyocardiumMyocytes, Smooth MuscleStreptozocinVentricular Dysfunction, LeftBlood GlucoseStreptozocinCardiac cellularityDiabetesEchocardiographyFibroblastFlow cytometry

Identifiers

PMID34074290
PMCPMC8170962
OpenAlexW3151891735

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.