| Project/Area Number |
16590663
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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 |
SUZUKI Jun-ichi Tokyo Medical and Dental University, Department of Cardiovascular Medicine, Junior Lecturer, 医学部附属病院, 助手 (90313858)
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| Co-Investigator(Kenkyū-buntansha) |
ISOBE Mitsuaki Tokyo Medical and Dental University, Department of Cardiovascular Medicine, Professor, 大学院・医歯学総合研究科, 教授 (80176263)
AMANO Jun Shinshu University, Department of Surgery, Professor, 医学部, 教授 (20138283)
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| Project Period (FY) |
2004 – 2005
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| Project Status |
Completed (Fiscal Year 2005)
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| Budget Amount *help |
¥3,500,000 (Direct Cost: ¥3,500,000)
Fiscal Year 2005: ¥1,700,000 (Direct Cost: ¥1,700,000)
Fiscal Year 2004: ¥1,800,000 (Direct Cost: ¥1,800,000)
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| Keywords | inflammation / myocardial ischemia / myocarditis / transplant rejection / restenosis / gene therapy / remodeling / clinical trial / 心臓移植 / 虚血再潅流傷害 / 動脈傷害 / NF-κB / カテキン / スタチン / HGF |
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| Research Abstract |
Background. Inflammation is a central event in cardiovascular diseases such as myocardial infarction, myocarditis, transplant rejection and arteriosclerosis after angioplasty. Methods and Results. To evaluate the effectiveness of blocking inflammation to prevent these diseases, we made several murine and rat experimental models. We showed that each treatment using a COX-2 inhibitor, pioglitazone, or tea catechins prevented acute and chronic cardiac rejection. We also demonstrated that treatment with a statin, a CCR1 antagonist, or a COX-2 inhibitor suppressed the rat autoimmune myocarditis. A specific I-kB inhibitor significantly suppressed ventricular remodeling after myocardial ischemia. An NF-kB decoy, an anti-E-selectin antibody, or an anti-VCAM-1 antibody suppressed arterial neointimal formation after arterial injury in a murine model. Based on these results, we performed clinical trials to prevent restenosis after PCI. Conclusion. Inflammation plays a pivotal role in cardiovascular diseases. These results suggest the clinical usefulness of gene therapies to regulate inflammatory cardiovascular diseases.
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