Elucidation of the mechanism of cardiomyopathy in CD36 deficiency and development of a novel therapy

2014 Fiscal Year Final Research Report

• Project/Area Number: 25860598
• Research Category: Grant-in-Aid for Young Scientists (B)
• Allocation Type: Multi-year Fund
• Research Field: Cardiovascular medicine
• Research Institution: Osaka University
• Principal Investigator: NAKATANI Kazuhiro 大阪大学, 医学(系)研究科(研究院), 特任研究員 (50648813)
• Project Period (FY): 2013-04-01 – 2015-03-31
• Keywords: 心筋エネルギー代謝 / CD36 / 心筋症 / iPS細胞

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.

Free Research Field

医学　循環器内科