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Functional Genomics Link REST to Endothelial Plasticity and Atherosclerosis.

Maria Viskadourou1, Sharjeel Chaudhry1, Arianna Scalco1

  • 1Division of Cardiology, Department of Medicine (M.V., S.C., A.S., P.R., P.T.-S., R.A., W.O., C.J.L., M.A.), Johns Hopkins University, Baltimore, MD.

Circulation Research
|November 26, 2025
PubMed
Summary
This summary is machine-generated.

Researchers discovered that the RE1-silencing transcription factor (REST) acts as a repressor in endothelial cells, preventing endothelial-to-mesenchymal transition and protecting against atherosclerosis. This finding offers new insights into coronary artery disease pathogenesis.

Keywords:
aortaatherosclerosiscoronary artery diseaseendothelial cellsgenomics

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Area of Science:

  • Genetics and Molecular Biology
  • Cardiovascular Research
  • Cell Biology

Background:

  • Genome-wide association studies (GWAS) have identified numerous loci associated with coronary artery disease (CAD) pathogenesis.
  • The underlying molecular mechanisms for these GWAS associations, particularly in endothelial cells, remain largely unexplored.

Purpose of the Study:

  • To prioritize endothelial-specific genetic loci associated with atherosclerosis using a multitrait colocalization approach.
  • To investigate the functional role of the identified locus targeting the RE1-silencing transcription factor (REST) gene in CAD.

Main Methods:

  • Applied a multitrait colocalization approach across expression quantitative trait loci (eQTLs) in atherosclerosis-relevant cell types.
  • Utilized in vitro CRISPR interference, Pcsk9-overexpressing mouse models with endothelial-specific Rest knockout, and RNA-sequencing (RNA-seq).
  • Performed single-nucleus RNA sequencing and Cleavage under Targets and Tagmentation (CUT&Tag) sequencing for mechanistic insights.

Main Results:

  • A conserved regulatory element in a chromosome 4 locus was found to increase CAD risk by decreasing REST expression in endothelial cells.
  • Endothelial-specific Rest knockout in mice led to increased atherosclerotic plaque formation, macrophage, and lipid deposition.
  • REST silencing in human aortic endothelial cells induced endothelial-to-mesenchymal transition (EndMT), increased permeability, and migration, involving L1CAM activation and TGFb signaling.

Conclusions:

  • RE1-silencing transcription factor (REST) acts as a crucial repressor in endothelial cells.
  • REST constitutively inhibits endothelial-to-mesenchymal transition (EndMT), thereby protecting against atherosclerosis.
  • These findings reveal a novel protective role for REST in cardiovascular health.