Evidence mapPaperPMID 38580969Full record

ArticleCardiovascular diabetology2024

Repressive H3K27me3 drives hyperglycemia-induced oxidative and inflammatory transcriptional programs in human endothelium.

Julia Sánchez-Ceinos, Shafaat Hussain, Abdul Waheed Khan, Liang Zhang, Wael Almahmeed, John Pernow, Francesco Cosentino

Open access · goldAbstract read
In one paragraph

Article in Cardiovascular diabetology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed, 1 pooled it
5.2field-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

25 citing papers in PubMed, 1 synthesis or guideline pooled it, 21 citations in OpenAlex.

  1. Pooled it
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  10. Epigenetic regulation in a high-sugar environment (Review).International journal of molecular medicine · 2026
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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

7 authors at 3 institutions in 3 countries.

Julia Sánchez-Ceinos *Cardiology Unit, Department of Medicine-Solna, Karolinska Institutet, Karolinska University Hospital, Stockholm, Sweden.
Shafaat Hussain *Cardiology Unit, Department of Medicine-Solna, Karolinska Institutet, Karolinska University Hospital, Stockholm, Sweden.
Abdul Waheed KhanCardiology Unit, Department of Medicine-Solna, Karolinska Institutet, Karolinska University Hospital, Stockholm, Sweden.
Liang ZhangCardiology Unit, Department of Medicine-Solna, Karolinska Institutet, Karolinska University Hospital, Stockholm, Sweden.
Wael AlmahmeedHeart and Vascular Institute, Cleveland Clinic Abu Dhabi, Abu Dhabi, UAE.
John PernowCardiology Unit, Department of Medicine-Solna, Karolinska Institutet, Karolinska University Hospital, Stockholm, Sweden.
Francesco CosentinoCardiology Unit, Department of Medicine-Solna, Karolinska Institutet, Karolinska University Hospital, Stockholm, Sweden. francesco.cosentino@ki.se.
Karolinska Institutet · SEKarolinska University Hospital · SECleveland Clinic · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundHistone modifications play a critical role in chromatin remodelling and regulate gene expression in health and disease. Histone methyltransferases EZH1, EZH2, and demethylases UTX, JMJD3, and UTY catalyse trimethylation of lysine 27 on histone H3 (H3K27me3). This study was designed to investigate whether H3K27me3 triggers hyperglycemia-induced oxidative and inflammatory transcriptional programs in the endothelium.

methodsWe studied human aortic endothelial cells exposed to high glucose (HAEC) or isolated from individuals with diabetes (D-HAEC). RT-qPCR, immunoblotting, chromatin immunoprecipitation (ChIP-qPCR), and confocal microscopy were performed to investigate the role of H3K27me3. We determined superoxide anion (O

resultsIncubation of HAEC to high glucose showed that upregulation of EZH2 coupled to reduced demethylase UTX and JMJD3 was responsible for the increased H3K27me3. ChIP-qPCR revealed that repressive H3K27me3 binding to superoxide dismutase and transcription factor JunD promoters is involved in glucose-induced O

conclusionsEZH2-mediated H3K27me3 represents a key epigenetic driver of hyperglycemia-induced endothelial dysfunction. Targeting EZH2 may attenuate oxidative stress and inflammation and, hence, prevent vascular disease in diabetes.

Indexed as

Diabetes MellitusHyperglycemiaAnimalsEndothelial CellsEndotheliumEnhancer of Zeste Homolog 2 ProteinGlucoseHistonesHumansMethylationMiceNF-kappa BEnhancer of Zeste Homolog 2 ProteinGlucoseHistonesNF-kappa BChromatin-modifying drugsDiabetesEndothelial cellsEpigeneticsEZH2 inhibitor GSK126InflammationOxidative stress

Identifiers

PMID38580969
PMCPMC10998410
OpenAlexW4393998087

What Socratic 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 Socratic graph.