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2016 Fiscal Year Final Research Report

Regulatory mechanism of mitochondrial morphology by Nox4 and treatment for heart failure

Research Project

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Project/Area Number 15K19358
Research Category

Grant-in-Aid for Young Scientists (B)

Allocation TypeMulti-year Fund
Research Field Cardiovascular medicine
Research InstitutionKyushu University (2016)
Hokkaido University (2015)

Principal Investigator

Matsushima Shoji  九州大学, 大学病院, 助教 (80552869)

Co-Investigator(Renkei-kenkyūsha) TSUTSUI Hiroyuki  九州大学, 大学院医学研究院・循環器内科学, 教授 (70264017)
KINUKAWA Shintaro  北海道大学, 大学院医学研究科・循環病態内科学, 講師 (60399871)
Research Collaborator MATSUMOTO Junichi  北海道大学, 大学院医学研究科・循環病態内科学, 大学院生
OKABE Kosuke  九州大学, 大学院医学研究院・循環器内科学, 大学院生
IKEDA Soichiro  九州大学, 大学院医学研究院・循環器内科学, 大学院生
Project Period (FY) 2015-04-01 – 2017-03-31
Keywords心筋リモデリング / 心不全 / ミトコンドリア / 酸化ストレス
Outline of Final Research Achievements

In failing myocardium, mitochondrial size was decreased and number of mitochondria was incraesed. These changes were accompanited by a decrease in phosphorylation of Drp1, a inhibitor form of Drp1, and an increase in Mitofusin1. Treatment with angioteisinII (AngII) increased active form of Drp1 in cardiomyoctyes. GKT137831, a inhibitor of Nox4, inhibited AngII-induced activation of Drp1. These results suggest that Nox4 is a regulator of Drp1 and involved in mitochondrial dynamics in cardiomyocytes.

Free Research Field

循環器内科学

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Published: 2018-03-22  

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