2015 Fiscal Year Final Research Report
The regulation mechanism of mitochondrial Ca2+ signaling and pathological mechanism of cardiovascular diseases for its abnormality
Project/Area Number |
26893317
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Research Category |
Grant-in-Aid for Research Activity Start-up
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Allocation Type | Single-year Grants |
Research Field |
General pharmacology
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Research Institution | Fukuoka University |
Principal Investigator |
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Project Period (FY) |
2014-08-29 – 2016-03-31
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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.
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Free Research Field |
循環器薬理学
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