Study on the pathogenesis of peripertum cardiomyopathy using genetically modified mouse model

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In this study, we established an animal model for "peripertum cardiomyopathy" (MHC-APJ) by cardiomyocyte-specific overexpression of APJ, a member of G-protein coupled receptor superfamily and expressing mainly in cardiovascular system. The lactating MHC-APJ mother exhibited reduced cardiac function, enlargement of the heart, cardiac fibrosis, and enhanced mRNA expression of the marker genes of heart failure. We found that "lactation" is essential for the pathogenesis of above phenotypes in MHC-APJ because those were not observed in non-pregnant or non-lactating MHC-APJ mother. By using an exhaustive gene expression analysis, we identified the several genes that changed only in the heart from lactating MHC-APJ mice. We consider these genes to be the candidates of the pathogenesis of peripertum cardiomyopathy induced by the combined action of enhanced APJ signaling and lactation in mice.