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2015 Fiscal Year Final Research Report

The regulation mechanism of mitochondrial Ca2+ signaling and pathological mechanism of cardiovascular diseases for its abnormality

Research Project

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Project/Area Number 26893317
Research Category

Grant-in-Aid for Research Activity Start-up

Allocation TypeSingle-year Grants
Research Field General pharmacology
Research InstitutionFukuoka University

Principal Investigator

TAGASHIRA Hideaki  福岡大学, 医学部, 助教 (90735028)

Project Period (FY) 2014-08-29 – 2016-03-31
Keywordsミトコンドリア / 心血管疾患
Outline of Final Research Achievements

Cardiovascular disease including heart failure is a one of the most important health problem owing to its significant morbidity and mortality. One of the most important factor causing heart disease including cardiac hypertrophy and heart failure is dysregulation of Ca2+ signaling. Recently, mitochondrial calcium uniporter (MCU) and mitochondrial Na+/Ca2+ exchanger (NCLX) was identified, and possessed mitochondrial Ca2+ signaling study in many different cells and organs. However, physiological and pathological roles of mitochondrial Ca2+ signaling in cardiovascular function are still unclear. To study the functional role of mitochondrial Ca2+ signaling in cardiovascular diseases, we developed NCLX and MCU-knockout mice. In this study using these mice, we found that the disruption of mitochondrial Ca2+ signaling contribute to the onset and progression of cardiovascular diseases.

Free Research Field

循環器薬理学

URL: 

Published: 2017-05-10  

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