| Project/Area Number |
24659385
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Single-year Grants |
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| Research Field |
Circulatory organs internal medicine
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| Research Institution | Nagoya University |
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Principal Investigator |
XIAN WU Cheng 名古屋大学, 医学(系)研究科(研究院), 特任准教授 (30378228)
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| Project Period (FY) |
2012-04-01 – 2014-03-31
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥3,770,000 (Direct Cost: ¥2,900,000、Indirect Cost: ¥870,000)
Fiscal Year 2013: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2012: ¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
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| Keywords | カテプシンK / 心房細動 / 心房リモデリング / マトリックス蛋白 / バイオマーカー |
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| Research Abstract |
We sought to determine the link between atrial fibrillation (AF) and plasma CatK levels and to investigate the expression and therapeutic target for CatK. Plasma levels of CatK were measured in patients with AF (paroxysmal AF [PAF]; persistent AF [PeAF]) and control subjects. AF had higher CatK than did controls. PeAF had higher CatK levels than PAF. CatK was correlated left atrial diameter in all subjects. The levels of atrial tissue angiotensin II, AT1R, gp91phox, p-p38MAPK, and CatK; O2-; and CatK activity; and fibrosis were greater in rabbits with AF than in that of controls, and these changes were reversed by AT1R blocker (ARB). Olmesartan decreased the CatK expression induced by angiotensin II in neonatal myocytes. These data indicated that increased plasma CatK levels are linked with the presence of AF. ARB appears to be effective in alleviating atrial fibrosis in a rabbit AF model, partly reducing AT1R-p38MAPK-dependent and -independent CatK activation, thus preventing AF.
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