| Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2014: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2013: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Outline of Final Research Achievements |
We analyzed wild type (WT) mice and CD36 knockout (KO) mice under the pressure overload due to transverse aortic constriction (TAC). By applying a TAC, the survival rate was significantly lower in KO than in WT mice. KO mice with TAC showed an increased hypertrophic and fibrotic changes in cardiomyocytes than in WT mice with TAC. KO with TAC showed reduced left ventricle fractional shortening and resulted in heart failure with systolic dysfunction. We prepared iPS cell from healthy control(n=5) and CD36 deficiency(n=4) with or without cardiomyopathy. We are inducing differentiation from iPS cells to cardiomyocytes. We are analyzing phenotype of cardiomyocytes derived from them. Moreover, we are developing a novel therapy for the abnormal cardiomyocytes derived from CD36 deficient patients with cardiomyopathy. We have reported these data in the scientific meetings and submitted as an original article written in English.
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