Evidence map›Paper›PMID 38446896›Full record

ArticleScience advances2024

Atlas of cardiac endothelial cell enhancer elements linking the mineralocorticoid receptor to pathological gene expression.

Lisa Deng, Luisa Pollmeier, Rebecca Bednarz, Can Cao, Patrick Laurette, Luisa Wirth, Argen Mamazhakypov, Christine Bode, Lutz Hein, Ralf Gilsbach and 1 more

Open access · goldAbstract read
In one paragraph

Article in Science advances, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
5.0field-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

4 citing papers in PubMed, 12 citations in OpenAlex.

  1. Cardiac epigenome in heart development and disease.Nature reviews. Cardiology · 2026
    Review
  2. 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

11 authors at 2 institutions in 1 country.

Lisa DengInstitute of Experimental and Clinical Pharmacology and Toxicology, Faculty of Medicine, University of Freiburg, Freiburg, Germany.ORCID 0009-0009-3846-2394
Luisa PollmeierInstitute of Experimental and Clinical Pharmacology and Toxicology, Faculty of Medicine, University of Freiburg, Freiburg, Germany.
Rebecca BednarzInstitute of Experimental Cardiology, Heidelberg University Hospital, Heidelberg, Germany.ORCID 0000-0003-2565-0459
Can CaoInstitute of Experimental Cardiology, Heidelberg University Hospital, Heidelberg, Germany.ORCID 0000-0001-8559-3535
Patrick LauretteInstitute of Experimental Cardiology, Heidelberg University Hospital, Heidelberg, Germany.ORCID 0000-0002-8941-612X
Luisa WirthInstitute of Experimental and Clinical Pharmacology and Toxicology, Faculty of Medicine, University of Freiburg, Freiburg, Germany.ORCID 0000-0002-8088-8892
Argen MamazhakypovInstitute of Experimental and Clinical Pharmacology and Toxicology, Faculty of Medicine, University of Freiburg, Freiburg, Germany.ORCID 0000-0002-2140-4819
Christine BodeInstitute of Experimental and Clinical Pharmacology and Toxicology, Faculty of Medicine, University of Freiburg, Freiburg, Germany.ORCID 0009-0008-5063-3910
Lutz HeinInstitute of Experimental and Clinical Pharmacology and Toxicology, Faculty of Medicine, University of Freiburg, Freiburg, Germany.ORCID 0000-0003-1297-0007
Ralf GilsbachInstitute of Experimental Cardiology, Heidelberg University Hospital, Heidelberg, Germany.ORCID 0000-0002-0895-1535
Achim LotherInstitute of Experimental and Clinical Pharmacology and Toxicology, Faculty of Medicine, University of Freiburg, Freiburg, Germany.ORCID 0000-0001-9107-5558
University of Freiburg · DEHeidelberg University · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Endothelial cells play crucial roles in physiology and are increasingly recognized as therapeutic targets in cardiovascular disease. Here, we analyzed the regulatory landscape of cardiac endothelial cells by assessing chromatin accessibility, histone modifications, and 3D chromatin organization and confirmed the functional relevance of enhancer-promoter interactions by CRISPRi-mediated enhancer silencing. We used this dataset to explore mechanisms of transcriptional regulation in cardiovascular disease and compared six different experimental models of heart failure, hypertension, or diabetes. Enhancers that regulate gene expression in diseased endothelial cells were enriched with binding sites for a distinct set of transcription factors, including the mineralocorticoid receptor (MR), a known drug target in heart failure and hypertension. For proof of concept, we applied endothelial cell-specific MR deletion in mice to confirm MR-dependent gene expression and predicted direct MR target genes. Overall, we have compiled here a comprehensive atlas of cardiac endothelial cell enhancer elements that provides insight into the role of transcription factors in cardiovascular disease.

Indexed as

AscomycotaCardiovascular DiseasesHeart FailureHypertensionAnimalsEndothelial CellsEnhancer Elements, GeneticGene ExpressionMiceReceptors, MineralocorticoidTranscription FactorsReceptors, MineralocorticoidTranscription Factors

Identifiers

PMID38446896
PMCPMC10917356
OpenAlexW4392502301

What Socratic holds

Textmetadata
LicenceCC BY-NC
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.