Pressure Overload Impairs Cardiac Function in Long-Chain Fatty Acid Transporter CD36-Knockout Mice
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- Nakatani Kazuhiro
- Department of Cardiovascular Medicine, Sumitomo Hospital
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- Masuda Daisaku
- Rinku Innovation Center for Wellness Care and Activities (RICWA), Health Care Center, Department of Cardiology, Rinku General Medical Center
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- Kobayashi Takuya
- Rinku General Medical Center
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- Sairyo Masami
- Department of Cardiovascular Medicine, Kawanishi City Hospital
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- Zhu Yinghong
- Department of Cardiovascular Medicine, Osaka University Graduate School of Medicine
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- Okada Takeshi
- Department of Cardiovascular Medicine, Osaka University Graduate School of Medicine
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- Naito Atsuhiko T.
- Department of Pharmacology, Faculty of Medicine, Toho University
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- Ohama Tohru
- Department of Cardiovascular Medicine, Osaka University Graduate School of Medicine Osaka University Dental Hospital
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- Koseki Masahiro
- Department of Cardiovascular Medicine, Osaka University Graduate School of Medicine Health Care Division, Health and Counseling Center, Osaka University
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- Oka Toru
- Department of Medical Checkup, Osaka International Cancer Institute
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- Akazawa Hiroshi
- Department of Cardiovascular Medicine, The University of Tokyo Graduate School of Medicine
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- Nishida Makoto
- Department of Cardiovascular Medicine, Osaka University Graduate School of Medicine Health Care Division, Health and Counseling Center, Osaka University
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- Komuro Issei
- Department of Cardiovascular Medicine, The University of Tokyo Graduate School of Medicine
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- Sakata Yasushi
- Department of Cardiovascular Medicine, Osaka University Graduate School of Medicine
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- Yamashita Shizuya
- Rinku General Medical Center Department of Cardiovascular Medicine, Osaka University Graduate School of Medicine Department of Community Medicine, Osaka University Graduate School of Medicine
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抄録
<p>CD36 is one of the important transporters of long-chain fatty acids (LCFAs) in the myocardium. We previously reported that CD36-deficient patients demonstrate a marked reduction of myocardial uptake of LCFA, while myocardial glucose uptake shows a compensatory increase, and are often accompanied by cardiomyopathy. However, the molecular mechanisms and functional role of CD36 in the myocardium remain unknown.</p><p>The current study aimed to explore the pathophysiological role of CD36 in the heart. Methods: Using wild type (WT) and knockout (KO) mice, we generated pressure overload by transverse aortic constriction (TAC) and analyzed cardiac functions by echocardiography. To assess cardiac hypertrophy and fibrosis, histological and molecular analyses and measurement of ATP concentration in mouse hearts were performed.</p><p>By applying TAC, the survival rate was significantly lower in KO than that in WT mice. After TAC, KO mice showed significantly higher heart weight-to-tibial length ratio and larger cross-sectional area of cardiomyocytes than those of WT. Although left ventricular (LV) wall thickness in the KO mice was similar to that in the WT mice, the KO mice showed a significant enlargement of LV cavity and reduced LV fractional shortening compared to the WT mice with TAC. A tendency for decreased myocardial ATP concentration was observed in the KO mice compared to the WT mice after TAC operation.</p><p>These data suggest that the LCFA transporter CD36 is required for the maintenance of energy provision, systolic function, and myocardial structure.</p>
収録刊行物
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- International Heart Journal
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International Heart Journal 60 (1), 159-167, 2019-01-31
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