2014 Fiscal Year Final Research Report
Molecular mechanisms of left ventricular diastolic dysfunction in the type 2 diabetic heart
| Project/Area Number |
25860611
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Cardiovascular medicine
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| Research Institution | Sapporo Medical University |
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Principal Investigator |
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| Project Period (FY) |
2013-04-01 – 2015-03-31
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| Keywords | 拡張機能 / 糖尿病 / 心不全 / AMP deaminase |
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| Outline of Final Research Achievements |
The aim of this study was to examine mechanisms by which type 2 diabetes (T2DM) augments ventricular diastolic stiffness in response to pressure overloading. We found that AMP deaminse activity was increased in T2DM hearts, resulting in excessive degradation of adenine nucleotides and ATP depletion during pressure overloading. ATP level was negatively correlated with tau of LV pressure and LVEDP. These diastolic properties were observed before development of extracellular matrix or titin remodeling.
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| Free Research Field |
医歯薬学
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