| Budget Amount *help |
¥5,200,000 (Direct Cost: ¥4,000,000、Indirect Cost: ¥1,200,000)
Fiscal Year 2013: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2012: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2011: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Research Abstract |
We found that cardiac injury and dysfunction after ischemia-reperfusion or doxorubicin administration were prevented in cardiac-specific gene knockout (KO) mice of SOCS3 (suppressor of cytokine signaling-3). To investigate the mechanism for the prevention of cardiac injury and dysfunction after ischemia-reperfusion or doxorubicin administration in cardiac-specific SOCS3-KO mice, we conducted microarray analysis. Microarray analysis revealed that apoptosis related genes and mitochondria and energy metabolism related genes were important for this prevention in SOCS3-KO mice. These results suggest that socs3, which is a negative regulator of Jak-STAT3 signaling pathway, is important for cardioprotection against stress-induced myocardial injury. SOCS3 may be a promising therapeutic target for acute myocardial infarction and heart failure.
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