Epigenetic regulation of gene expression related to compensated myocardial hypertrophy under pressure overload

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The mechanism of disruption of compensated myocardial hypertrophy under excessive pressure overload has not been fully clarified. We previously described that low level of IL-1 is constitutively produced and IL-1 induce IGF-1 to maintain homeostasis of cardiomyocyte under pressure overload. In this report, we addressed the epigenetic regulatory mechanism to control expression of genes which is involved in the transition of compensated hypertrophy to dilated heart failure. As a result, during the transition phase of compensated hypertrophy to decompensated dilated heart failure, methylation of IGF-1 promoter was increased. Furthermore, in vivo administration of DNA methyl-transferase inhibitors increases expression level of IGF-1 and inhibited transition of compensated hypertrophy to dilated heart failure.