| Project/Area Number |
09281103
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| Research Category |
Grant-in-Aid for Scientific Research on Priority Areas (A)
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| Allocation Type | Single-year Grants |
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| Research Institution | KYOTO UNIVERSITY |
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Principal Investigator |
KITA Toru Kyoto University Professor, 医学研究科, 教授 (60161460)
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| Co-Investigator(Kenkyū-buntansha) |
YAMADA Nobuhiro Tsukuba University Professor, 臨床医学系, 教授 (40200729)
MATSUZAWA Yuji Osaka University Professor, 医学系研究科, 教授 (70116101)
HORIUCHI Seikoh Kumamoto University Professor, 医学部, 教授 (10117377)
ANDO Joji Tokyo University Professor, 医学系研究科, 教授 (20159528)
MARUYAMA Ikuro Kagoshima University Professor, 医学部, 教授 (20082282)
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| Project Period (FY) |
1997 – 2000
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| Project Status |
Completed (Fiscal Year 2001)
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| Budget Amount *help |
¥200,100,000 (Direct Cost: ¥200,100,000)
Fiscal Year 2000: ¥53,100,000 (Direct Cost: ¥53,100,000)
Fiscal Year 1999: ¥51,600,000 (Direct Cost: ¥51,600,000)
Fiscal Year 1998: ¥47,700,000 (Direct Cost: ¥47,700,000)
Fiscal Year 1997: ¥47,700,000 (Direct Cost: ¥47,700,000)
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| Keywords | Atherosclerosis / Vascular endothelial cell / Vasculogenesis / Angiogenesis / Vascular smooth muscle cell / Phenotypic conversion / Adhesion molecule / Oxidized LDL / リゾフォスファチジルコリン / CD36 / LOX-1 / マクロファージ / ずり応力 / 酸化LDL受容体 |
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| Research Abstract |
The Grants-in-Aid for Scientific Research on Priority Areas No. 09281104 was issued from 1997 to 2000. During the period, we organized a research group with scientists who are considered to be most active in the research field. Atherosclerosis is correlated with a variety of vascular disorders such as coronary heart disease. We therefore placed our goal on elucidation of the molecular mechanism of atherosclerosis and exploration of novel therapeutic strategies. To conduct investigation, the members were divided into 3 subgroups, i.e. Group 1, 2, and 3 with different subject of study as follows. We also formed a Central Committee to coordinate and facilitate the research activity of the subgroups.
The Study Group 3 studied endothelial dysfunction and blood cells. There has been accumulating evidence that atherosclerosis is initiated by endothelial dysfunction due to a variety of biological insults. We therefore formed this subgroup to explore the key molecules involved in those events. We discovered novel scavenger receptors such as LOX-1 and SRPSOX. Furthermore, we revealed that adipose tissues produce cytokines abundantly. Among those cytokines, adiponectin has been shown to play an important role in atherogenesis and insulin resistance.
In conclusion, we have made a successful progress in atherosclerosis research, which will be translated into clinical application in the near future.
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