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. 2022 Jan 21;12(2):172. doi: 10.3390/biom12020172

Table 2.

Epigenetic modifications in endothelial cells in AAAs.

Epigenetic Modification Cellular Origin Regulation Target Gene(s) Related Function
Histone Modification
BRG1 Endothelial cell COL1A1, COL1A2, vimentin Promotes AAA formation upregulation of fibrotic gene expression
HDAC9 Endothelial cell Enhances endothelial-to-mesenchymal transition
Non-coding RNAs
miRNA-20a Endothelial cell Upregulated PTEN, ATG7 Inhibits endothelial cell apoptosis
miRNA-21 Endothelial cell Upregulated
miRNA-27a Endothelial cell Upregulated SEMA6A Promotes endothelial-to-mesenchymal transition
miRNA-92a Endothelial cell Upregulated KLF4 Secreted by EC, inhibits KLF4 expression in macrophages; enhances atherosclerotic lesion formation
miRNA-126 Endothelial cell Upregulated ADAM9 Overexpression reduces AAA formation; suppression of inflammatory cytokines
miRNA-221 Endothelial cell Upregulated CDKN1B, PIK3R1 Promotes angiogenesis via regulating endothelial tip-cell proliferation and migration
miRNA-222 Endothelial cell Upregulated ADIPOR1 Overexpression promotes AAA by interfering with endothelial progenitor cell function
Let-7 (miRNA) Endothelial cell Upregulated
GATA6-AS (lncRNA) Endothelial cell Upregulated? LOXL2 Inhibition of TGFβ2-mediated endothelial-to-mesenchymal transition
H19 (lncRNA) Endothelial cell Inhibition of endothelial-to-mesenchymal transition
MALAT-1 (lncRNA) Endothelial cell NOX2 Increased inflammation and ROS production
SENCR (lncRNA) Endothelial cell CKAP4 Stabilizes vascular EC adherens junctions

AAA, abdominal aortic aneurysm; EC, endothelial cell; ROS, reactive oxygen species.