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From the Department of Internal Medicine and Cardiology (T.O., M.Y., Y.N., M.T., K.T., J.Y.), Department of Pharmacology (H.I.), Department of Hepatology (S.N., K.F.), Osaka City University Medical School, Osaka; Third Department of Medicine (T.H., S.I., Y.K.), Osaka Medical College, Osaka; the Third Department of Internal Medicine (M.K., S.H.), Mie University School of Medicine, Mie; and the Department of Developmental Genetics (T.T.), Chiba University Graduate School of Medicine, Chiba, Japan.
Correspondence to Takashi Omura, Department of Internal Medicine and Cardiology, Osaka City University Medical School, 1-4-3 Asahimachi, Abeno-ku, Osaka 545-8585, Japan. E-mail omura{at}med.osaka-cu.ac.jp
Hepatitis C virus (HCV) has been reported to be associated with cardiomyopathy. However, the mechanism of cardiomyopathy in chronic HCV infection is still unclear. Therefore, we investigate the development of cardiomyopathy in mice transgenic for the HCV-core gene. After the age of 12 months, mice developed cardiomyopathy that appeared as left ventricular dilatation, and systolic and diastolic dysfunction assessed by Doppler echocardiography. Histologically, hypertrophy of cardiomyocytes, cardiac fibrosis, disarray and scarcity of myofibrils, vacuolization and deformity of nuclei, myofibrillar lysis, streaming of Z-bands, and an increased number of bizarre-shaped mitochondria were found in HCV-core transgenic mice. These histological changes are just consistent with cardiomyopathy. In conclusion, the HCV-core protein directly plays an important role in the development of cardiomyopathy.
Key Words: hepatitis C virus core protein cardiomyopathy
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