ArticleArteriosclerosis, thrombosis, and vascular biology2024
Coronary Artery Disease Risk Variant Dampens the Expression of CALCRL by Reducing HSF Binding to Shear Stress Responsive Enhancer in Endothelial Cells In Vitro.
Article in Arteriosclerosis, thrombosis, and vascular biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Novel Role for CGRP in Aqueous Humor Outflow.Investigative ophthalmology & visual science · 2026Article
- Epigenetic regulation in atherosclerosis and its therapeutic potential.Nature reviews. Cardiology · 2026Review
- Multi-omics integration reveals the role of N6-methyladenosine in epilepsy, ischemic stroke, and vascular dementia.Molecular brain · 2025Article
- Endothelial gene regulatory elements associated with cardiopharyngeal lineage differentiation.Communications biology · 2024Article
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Authors and funding
22 authors.
Funding
Abstract
backgroundCALCRL (calcitonin receptor-like) protein is an important mediator of the endothelial fluid shear stress response, which is associated with the genetic risk of coronary artery disease. In this study, we functionally characterized the noncoding regulatory elements carrying coronary artery disease that risks single-nucleotide polymorphisms and studied their role in the regulation of
methodsTo functionally characterize the coronary artery disease single-nucleotide polymorphisms harbored around the gene
resultsWe demonstrate that the regulatory element harboring rs880890 exhibits high enhancer activity and shows significant allelic bias. The A allele was favored over the G allele, particularly under shear stress conditions, mediated through alterations in the HSF1 (heat shock factor 1) motif and binding. CRISPR deletion of rs880890 enhancer resulted in downregulation of
conclusionsOverall, our results demonstrate the existence of an endothelial-specific HSF (heat shock factor)-regulated transcriptional enhancer that mediates
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