| Budget Amount *help |
¥18,460,000 (Direct Cost: ¥14,200,000、Indirect Cost: ¥4,260,000)
Fiscal Year 2015: ¥5,590,000 (Direct Cost: ¥4,300,000、Indirect Cost: ¥1,290,000)
Fiscal Year 2014: ¥5,850,000 (Direct Cost: ¥4,500,000、Indirect Cost: ¥1,350,000)
Fiscal Year 2013: ¥7,020,000 (Direct Cost: ¥5,400,000、Indirect Cost: ¥1,620,000)
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| Outline of Final Research Achievements |
In this study, identification of gene abnormalities in hereditary cardiomyopathy and their pathogenesis were invesigated. It was revealed that the increased calcium sensitivity could directly cause hypertrophic cardiomyopathy in a mouse model and its pathogenesis was inhibited by a ROCK2 inhibirtor. In addition, molecular mechanisms for gender differences in dilated cardiomyopathy caused by lamin A/C gene mutations was found to involve transport of androgen receptor with FHL2 resulting in SRF-mediated expression of genes for cardiac remodeling. Moreover, several novel disease genes for hereditary cardiomyopathy were identified by a linkage study in a large multiplex family with hypertrophic cardiomyaopathy and by candidate gene approaches for hypertrophic cardiomyopathy and dilated cardiomyopathy. Functional abnormalities caused by the mutations in these novel disease genes were also investigated to reveal the molecular pathogenesis of cardiomyopathies.
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