Table 1.

The Role of DNA methylation in CAVD/Aortic Stenosis.

Observation in CAVD/AS	Effect	Species	References
Increased levels of DNMT3B in human stenotic aortic valves	Increase in global DNA methylation. More than 6,000 differentially methylated sites were identified between normal and stenotic valves. Expression of the osteogenic marker Sp7 was increased four-fold in stenotic vs. normal tissue	Human	(156)
Genetic inactivation of DNMT3B	Protects against activation of osteogenic pathways and slows the progression of aortic stenosis	Mouse	(157)
Altered CpG methylation in newborns with congenital aortic stenosis	Differentially methylated CpG sites	Human	(158)
Altered methylation of CpG sites	Contribution to regulation of left ventricular hypertrophy due to aortic stenosis -induced pressure overload	Human	(159)
Hypomethylation of LncRNA H19	Promotes VIC osteogenic-like changes by NOTCH1 silencing	Human	(160)
5-methylcytosine (5meC) in intron 1 in a mammalian interspersed repeat element (MIR) was increased by 2.2-fold in CAVD compared to control aortic valves	Phospholipid phosphatase (PLPP3) gene and enzymatic activity were downregulated in mineralized aortic valves	Human	(161)
Decreased promoter methylation of the gene encoding the proinflammatory enzyme 5-lipoxygenase (5-LO)	Increased 5-LO mRNA levels. (Aortic stenosis is associated with increased leukotriene production, in part, due to induction of 5-LO in VICs)	Human	(162)