2016 Fiscal Year Final Research Report
DPP4 inhibition ameliorates cardiac function by blocking the cleavage of HMGB1 in diabetic mice after myocardial infarction
| Project/Area Number |
15K19390
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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 | Fukushima Medical University |
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Principal Investigator |
Yuichi Nakamura 福島県立医科大学, 医学部, 博士研究員 (10745798)
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| Project Period (FY) |
2015-04-01 – 2017-03-31
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| Keywords | DPP4 inhibitor / Myocardial infarction / HMGB1 / cardiac remodeling / angiogenesis |
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| Outline of Final Research Achievements |
DPP4 activity was increased in the diabetic state and blocked by anagliptin administration. The HMGB1 plasma levels were reduced in the diabetic TG compared with the non-diabetic TG mice, but DPP4 inhibition with anagliptin 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 MI.
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| Free Research Field |
Cardiology
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