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. Author manuscript; available in PMC: 2015 Jun 20.
Published in final edited form as: Circ Res. 2014 Apr 22;115(1):32–43. doi: 10.1161/CIRCRESAHA.115.303883

Figure 7. Summary schematic of KLF4 promoter methylation mechanisms contributing to suppression of transcription.

Figure 7

DF-induced DNMT3A enrichment of endothelial KLF4 promoter near the TSS increased CpG methylation. Hypermethylation prevented MEF2-complex binding resulting in inhibition of KLF4 transcription. Decreased KLF4 expression can lower the interaction of KLF4 with its transcription targets independently of their methylation status leading to a pro-inflammatory, pro-atherosclerosis phenotype. Intervention by DNMT inhibitors (RG108; 5-Aza) can rescue this pathway.