| Project/Area Number |
22590825
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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 | Tokyo Medical and Dental University |
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Principal Investigator |
SAWADA Naoki 東京医科歯科大学, 歯と骨のGCOE拠点, GCOE拠点形成特任教員 (40343751)
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| Co-Investigator(Renkei-kenkyūsha) |
SATA Masataka 徳島大学, ヘルスバイオサイエンス研究, 教授 (80345214)
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| Research Collaborator |
ZOLT Arany Beth Israel Deaconess Medical Center, Harvard Medical School, Associate Professor of Medicine
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| Project Period (FY) |
2010 – 2012
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| Project Status |
Completed (Fiscal Year 2012)
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| Budget Amount *help |
¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2012: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2011: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2010: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | 分子血管病態学 / 血管新生 / 転写コアクチベータ |
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| Research Abstract |
Critical limb ischemia, the leading cause oflimb amputation, affects 10-15%ofdiabetic population, thus calling for critical needs to develop effective therapeutic means. The high prevalence oflimb ischemia in diabetes is in significant part caused by the inability of diabetics to elaborate new blood vessels (the process called angiogenesis) to resume blood supply in ischemic tissues. However, the underlying mechanism fbr this has been largely undefined. In the present study, we demonstrated that diabetes increases the abundance oftranscriptional co-activator PGC-1αin endothelial cells, which then renders endothelial cells unresponsive to angiogenic factors, and causes diminished angiogenic capacity in diabetes.
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