| Project/Area Number |
23590256
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
General physiology
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| Research Institution | Akita University |
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Principal Investigator |
IINO Kenji 秋田大学, 医学部, 講師 (30400485)
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| Co-Investigator(Kenkyū-buntansha) |
WATANABE Hiroyuki 秋田大学, 大学院医学系研究科, 准教授 (80323145)
ITO Hiroshi 秋田大学, 大学院医学系研究科, 教授 (10232464)
KOYAMA Takashi 秋田大学, 医学部, 助教 (50508273)
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| Project Period (FY) |
2011 – 2013
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥5,200,000 (Direct Cost: ¥4,000,000、Indirect Cost: ¥1,200,000)
Fiscal Year 2013: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2012: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2011: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
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| Keywords | 心房細動 / イオンチャネル / TRPチャネル / ＴＲＰチャネル |
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| Research Abstract |
Studies of transient receptor potential (TRP) channels have significantly extended our knowledge regarding the molecular basis of Ca2+ signals in cardiac myocytes. The functional significance of cardiac TRP channels is likely connected to the alteration of membrane potential or Ca2+ entry into a noncontractile compartment, where gene expression responsible for various cardiac diseases is induced. This study highlights some aspects of TRP channels with anticipated roles in cardiac disease. Evidence suggests that (a) increased activities of TRPC1, TRPC3, or TRPC6 are involved in the development of cardiac hypertrophy, where these TRPC channels act as unique sensors for a wide range of hypertrophic stimuli, and (b) increased activities of TRPM4,7 and TRPC3,6 are involved in atrial remodeling or mechanical stretch on cardiac arrhythmia. Ultimately, TRP channels may become novel pharmacological targets in the treatment of human cardiac disease.
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