| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2012: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2011: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2010: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
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| Research Abstract |
Type 5 adenylyl cyclase (AC5)is a major cardiac isoform and AC5 null mice show the resistance to oxidative stress and heart failure. Recent studies have shown that cAMP can activate Epac1, exchange protein directly activated by cAMP, as well. However, its role in the pathogenesis of heart failure remains unknown. In order to examine the role of Epac1 in the heart, we have generated the cardiac-specific type 5 adenylyl cyclase, a major cardiac AC isoform, transgenic mice (AC5TG) and Epac1-deficient AC5TG (AC5TG-EpacKO) and demonstrated that cAMP-Epac1 pathway plays an important role for the development of heart failure through the activation of cAMP-PKA pathway, suggesting that this pathway may be a new target for the treatment of heart failure.
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