| Project/Area Number |
12136101
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| Research Category |
Grant-in-Aid for Scientific Research on Priority Areas
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| Allocation Type | Single-year Grants |
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| Review Section |
Biological Sciences
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| Research Institution | Chiba University |
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Principal Investigator |
KOMURO Issei Chiba University, Graduate School of Medicine, Professor, 大学院医学研究院, 教授 (30260483)
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| Co-Investigator(Kenkyū-buntansha) |
TAKIHARA Keiko Osaka University, Health Care Center, Associate Professor, 保健センター, 助教授 (70252640)
MATSUBARA Hiroaki Kyoto Prefectural University of Medicine, Professor, 大学院医学研究科, 教授 (10239072)
SAITO Yoshihiko Nara Medical University, Professor, 医学部, 教授 (30250260)
MUROHARA Toyoaki Nagoya University, Graduate School of Medicine, Professor, 大学院医学系研究科, 教授 (90299503)
FUKUDA Keiichi Keio University, School of Medicine, Professor, 医学部, 教授 (20199227)
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| Project Period (FY) |
2000 – 2005
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| Project Status |
Completed (Fiscal Year 2005)
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| Budget Amount *help |
¥33,300,000 (Direct Cost: ¥33,300,000)
Fiscal Year 2005: ¥1,500,000 (Direct Cost: ¥1,500,000)
Fiscal Year 2004: ¥7,400,000 (Direct Cost: ¥7,400,000)
Fiscal Year 2003: ¥7,400,000 (Direct Cost: ¥7,400,000)
Fiscal Year 2002: ¥8,500,000 (Direct Cost: ¥8,500,000)
Fiscal Year 2001: ¥8,500,000 (Direct Cost: ¥8,500,000)
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| Keywords | heart failure / angiotensin II / STAT3 / bone marrow stem cell / ANP / cardiogenesis / regenerative medicine / 血管新生 / ANP / BNP / angiopoietin-1 / ErbB / gp130 / アンジオテンシンII受容体 / エンドセリン / NGF / NRSF / EGF / STAT / 骨髄細胞 / 骨髄単核球細胞 / CMG細胞 / 移植 / AT2 / GC-A / GFP / DNA chip |
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| Research Abstract |
Heart failure is a leading cause of death in industrialized nations. Although the mainstay of treatment is pharmacotherapy including treatment with angiotensin-converting enzyme inhibitors, angiotensin II receptor blockers and β-blockers, 1-year mortality is nearly 20% even with optimal medical therapy. Because other treatment options such as heart transplantation, ventricular assist devices and artificial hearts are not readily available to most patients, there has been a tremendous need for the development of novel treatment strategies for heart failure. As genetically altered mouse models are valid for investigating heart failure, we analyzed molecular mechanisms of heart failure using the mouse models. Furthermore, we investigated the mechanisms of cardiac regeneration to develop the novel strategies such as gene therapy, cell-based therapy and cytokine therapy.
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