| Project/Area Number |
18590762
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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, Assistant Professor (90313858)
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| Co-Investigator(Kenkyū-buntansha) |
INAGAKI Hiroshi Tokyo Medical and Dental University, Department of Cardiovascular Medicine, Junior Lecturer (60376803)
SAKURAI Kaoru National Disaster Medical Center, Department of Cardiovascular Medicine, Medical Doctor (70376771)
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| Project Period (FY) |
2006 – 2007
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| Project Status |
Completed (Fiscal Year 2007)
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| Budget Amount *help |
¥4,010,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥510,000)
Fiscal Year 2007: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
Fiscal Year 2006: ¥1,800,000 (Direct Cost: ¥1,800,000)
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| Keywords | inflammation / cardiac transplantation / myocarditis / myocardial ischemia / arteriosclerosis / gene transfer / animal models / clinical trial / 心筋梗塞 / 急性冠症候群 / リモデリング / 歯周病 / 遺伝子治療 |
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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 clarithromycin, pitavastatin, pioglitazone, or tea catechins prevented acute and chronic cardiac rejection. We also demonstrated that treatment with tea catechins, a CCR1 antagonist, or a COX-2 inhibitor suppressed the rat autoimmune myocarditis. A specific I-kB inhibitor or tea catechins significantly suppressed ventricular remodeling after myocardial ischemia. An NF-kB decoy 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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