| Project/Area Number |
14570661
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Circulatory organs internal medicine
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| Research Institution | OSAKA UNIVERSITY |
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Principal Investigator |
HIRAOKA Hisatoyo Osaka University Graduate School of Medicine, Assistant Professor, 医学系研究科, 助手 (00273681)
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| Co-Investigator(Kenkyū-buntansha) |
ISHIGAMI Masato Osaka University Hospital, Medical Staff, 医学部附属病院, 医員(臨床研究)
HIRANO Ken-ichi Osaka University Graduate School of Medicine, Assistant Professor, 医学系研究科, 助手 (30332737)
YAMASHITA Shizuya Osaka University Graduate School of Medicine, Associate Professor, 医学系研究科, 助教授 (60243242)
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| Project Period (FY) |
2002 – 2003
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| Project Status |
Completed (Fiscal Year 2003)
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| Budget Amount *help |
¥3,300,000 (Direct Cost: ¥3,300,000)
Fiscal Year 2003: ¥1,200,000 (Direct Cost: ¥1,200,000)
Fiscal Year 2002: ¥2,100,000 (Direct Cost: ¥2,100,000)
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| Keywords | NOS / Atherosclerosis / Nuclear receptors / CD36 / Genetic background / NO / 動脈硬化 / マクロファージ |
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| Research Abstract |
CD36, originally identified as glycoprotein IV on platelets, is an 88 kDa integral membrane protein that has multiple ligands and is expressed in the cardiovascular system (ie, blood vessel walls and the heart) as well as adipose tissues and skeletal muscles. Human genetic deficiency is relatively frequent in Asian and African populations. The investigation into the pathophysiology of this disorder has shown that CD36 may play an important role as a major scavenger receptor for oxidized low density lipoproteins and as a crucial transporter for long chain fatty acids. CD36 mediates intracellular signaling through some of important nuclear receptors such as NF-kB and PPARg and regulates inflammatory cytokines as well as inducible NOS. These results suggested that CD36 may play important roles in the pathogenesis of atherosclerosis.
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