| Project/Area Number |
15K09143
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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 |
Cardiovascular medicine
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| Research Institution | Fukushima Medical University |
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Principal Investigator |
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| Research Collaborator |
SUZUKI Satoshi 福島県立医科大学, 医学部, 助教 (60536944)
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| Project Period (FY) |
2015-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2017: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2016: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2015: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
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| Keywords | Myocardial infarction / Heart failure / Diabetes mellitus / HMGB1 / DPP4 / myocardial infarction / heart failure / diabetes mellitus |
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| Outline of Final Research Achievements |
In transgenic mice with cardiac-specific overexpression of HMGB1 (TG) and wild type mice (WT), a diabetic state was induced by streptozotocin, and myocardial infarction was created by ligation of the left anterior descending coronary artery. A dipeptidyl peptidase 4 (DPP4) inhibition increased HMGB1 plasma levels in the diabetic TG mice. The infarct area was significantly larger in the diabetic TG than in the non-diabetic TG mice, and was reduced by DPP4 inhibition. Cardiac function, angiogenesis, and VEGF expression were impaired in the diabetic TG mice, but ameliorated by the DPP4 inhibition to levels similar to those found in the non-diabetic TG mice.
The DPP4 inhibitor ameliorated cardiac function by inhibiting the inactivation of HMGB1 in diabetic mice after myocardial infarction.
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