Pathophysiological role of TRPV2 as a therapeutic target for cardiomyopathy/heart failure
Project/Area Number |
20590874
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Circulatory organs internal medicine
|
Research Institution | National Cardiovascular Center Research Institute |
Principal Investigator |
IWATA Yuko National Cardiovascular Center Research Institute, 分子生理部, 室長 (80171908)
|
Project Period (FY) |
2008 – 2010
|
Project Status |
Completed (Fiscal Year 2010)
|
Budget Amount *help |
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2010: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2009: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2008: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
|
Keywords | 心筋症 / 心不全 / イオンチャネル / カルシウム / 伸展刺激感受性チャネル / 筋変性 / 筋ジストロフィー / 機能的抗体 |
Research Abstract |
We identified TRPV2 as a principal candidate for Ca^<2+>-entry pathways which result in abnormal Ca^<2+> handling in muscular degeneration caused by cytoskeleton abnormality. Inhibition of endogenous TRPV2 significantly reduced the increase in basal intracellular Ca^<2+> and stretch-induced damage as well as improved muscle function in animal models. These data suggest that enhanced TRPV2 activity is important to trigger muscle damage and that it is a promising therapeutic target for muscular dystrophy and cardiomyopathy.
|
Report
(4 results)
Research Products
(39 results)