Evidence map›Paper›PMID 37924123›Full record

ArticleCardiovascular diabetology2023

Non-coding RNA-mediated endothelial-to-mesenchymal transition in human diabetic cardiomyopathy, potential regulation by DNA methylation.

Eric Wang, Shali Chen, Honglin Wang, Tori Chen, Subrata Chakrabarti

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cardiovascular diabetology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
2.9field-weighted citation impact, top 8% 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

13 citing papers in PubMed, 13 citations in OpenAlex.

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  8. Endothelial to mesenchymal transition: a central mechanism in diabetes-induced vascular pathology.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2025
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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

5 authors at 1 institution in 1 country.

Eric WangDepartment of Pathology and Laboratory Medicine, Western University, Dental Science Building Room 4033, 1151 Richmond St, London, ON, N6A 3K7, Canada.
Shali ChenDepartment of Pathology and Laboratory Medicine, Western University, Dental Science Building Room 4033, 1151 Richmond St, London, ON, N6A 3K7, Canada.
Honglin WangDepartment of Pathology and Laboratory Medicine, Western University, Dental Science Building Room 4033, 1151 Richmond St, London, ON, N6A 3K7, Canada.
Tori ChenDepartment of Pathology and Laboratory Medicine, Western University, Dental Science Building Room 4033, 1151 Richmond St, London, ON, N6A 3K7, Canada.
Subrata ChakrabartiDepartment of Pathology and Laboratory Medicine, Western University, Dental Science Building Room 4033, 1151 Richmond St, London, ON, N6A 3K7, Canada. subrata.chakrabarti@schulich.uwo.ca.
Western University · CA

Funding

CIHR 173414
6 · The paper itself

Abstract

aimsDiabetic cardiomyopathy (DCM) is a major complication of diabetes and a risk factor for cardiovascular disease. Endothelial dysfunction is central to DCM, and endothelial-to-mesenchymal transition (EndMT) is a key form of endothelial dysfunction in diabetes. EndMT in DCM has been well-studied in model systems and has been found to be epigenetically regulated by non-coding RNAs (ncRNAs). However, EndMT in DCM and its associated epigenetic changes need further characterization in human patients. It is also not known if ncRNAs are affected by changes in DNA methylation in DCM. This study aims to confirm in human hearts, the findings from animal and cell studies, and potentially provide novel insight into interactions between DNA methylation and ncRNAs in EndMT in DCM. METHODS AND

resultsHeart tissues were collected from autopsy patients, fixed in formalin, and embedded in paraffin. Thin sections from paraffin-embedded tissues were used for histology and immunofluorescence analyses, where we confirmed that diabetic patients showed increased cardiac fibrosis that EndMT had occurred. Tissue curls from the paraffin-embedded tissues were used for RT-qPCR and methylation analyses. RT-qPCR quantitatively showed that EndMT occurs in the hearts of diabetics, and that EndMT in human hearts corresponded to changes in key ncRNAs. Methylation analysis showed that some of the EndMT-related ncRNAs were regulated by DNA promoter methylation, while others may be regulated through different epigenetic mechanisms.

conclusionsWe show that EndMT is a relevant pathological process in human hearts during DCM, and that its occurrence coincides with changes in relevant ncRNAs. We further find that interplay between DNA methylation and certain ncRNAs involved in the regulation of EndMT may contribute to the observed changes in ncRNA expression. These findings reinforce the role of EndMT in patients afflicted with DCM and underscore the complexities and importance of the interactions between different facets of epigenetic regulation.

Indexed as

Diabetes MellitusDiabetic CardiomyopathiesAnimalsDNA MethylationEndotheliumEpigenesis, GeneticEpithelial-Mesenchymal TransitionHumansRNA, UntranslatedRNA, UntranslatedDiabetic cardiomyopathyEndothelial-to-mesenchymal transitionEpigeneticsLong non-coding RNAmicroRNAPromoter methylation

Identifiers

PMID37924123
PMCPMC10625293
OpenAlexW4388283635

What Socratic holds

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LicenceCC BY
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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 Socratic graph.