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2016 Fiscal Year Final Research Report

DPP4 inhibition ameliorates cardiac function by blocking the cleavage of HMGB1 in diabetic mice after myocardial infarction

Research Project

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Project/Area Number 15K19390
Research Category

Grant-in-Aid for Young Scientists (B)

Allocation TypeMulti-year Fund
Research Field Cardiovascular medicine
Research InstitutionFukushima Medical University

Principal Investigator

Yuichi Nakamura  福島県立医科大学, 医学部, 博士研究員 (10745798)

Project Period (FY) 2015-04-01 – 2017-03-31
KeywordsDPP4 inhibitor / Myocardial infarction / HMGB1 / cardiac remodeling / angiogenesis
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.

Free Research Field

Cardiology

URL: 

Published: 2018-03-22  

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