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Updated: Apr 16, 2026

A Chromatin Immunoprecipitation Assay to Identify Novel NFAT2 Target Genes in Chronic Lymphocytic Leukemia
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ZNF827 pleiotropic cardiovascular risk locus involves regulation by nuclear factor-1.

Yingwei Liu1, Lu Liu1,2,3, Asraa Esmael1

  • 1Université Paris Cité, Inserm, PARCC, F-75015 Paris, France.

Clinical Science (London, England : 1979)
|April 15, 2026
PubMed
Summary

A common genetic variant, rs13128814, influences Spontaneous Coronary Artery Dissection (SCAD) risk by affecting ZNF827 gene expression in vascular cells, potentially impacting multiple cardiovascular traits.

Keywords:
Functional genomicsgenetic risk cardiovascular diseasespontaneous coronary artery dissectiontranscriptional regulation

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Area of Science:

  • Genetics
  • Cardiovascular Biology
  • Molecular Biology

Background:

  • Spontaneous Coronary Artery Dissection (SCAD) predominantly affects middle-aged women, causing myocardial infarction via intramural hematoma and heart ischemia.
  • The ZNF827 locus on chromosome 4 is a known genetic risk factor for SCAD and other cardiovascular traits, but its molecular mechanisms remain unclear.

Purpose of the Study:

  • To elucidate the molecular mechanisms linking the ZNF827 locus to SCAD and related cardiovascular conditions.
  • To identify the specific genetic variant and regulatory elements involved in SCAD risk associated with the ZNF827 locus.

Main Methods:

  • Analysis of genetic associations and epigenetic markers.
  • Reporter assays in vascular smooth muscle cells (SMCs) to assess variant effects on gene transcription.
  • In silico prediction and experimental validation of transcription factor binding (NF1).
  • Gene knockdown studies in human iPSC-derived SMCs and fibroblasts to evaluate ZNF827 function.

Main Results:

  • The SCAD genetic risk locus colocalizes with a common intronic variant, rs13128814, overlapping with epigenetic markers in vascular cells.
  • The SCAD-risk allele (rs13128814-A) increases transcriptional activity in SMCs, with evidence suggesting Nuclear Factor-1 (NF1) binding.
  • ZNF827 knockdown in SMCs and fibroblasts dysregulated genes involved in macroautophagy and insulin signaling pathways.

Conclusions:

  • The rs13128814 variant, potentially mediated by NF1, influences ZNF827 expression, providing a molecular basis for its association with SCAD and other cardiovascular risks.
  • ZNF827 may function as a broad gene regulator in vascular SMCs and fibroblasts, contributing to arterial fragility in SCAD and related diseases.