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 |
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| Research Field |
General pharmacology
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| Research Institution | Fukuoka University |
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Principal Investigator |
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| Project Period (FY) |
2014-08-29 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥2,730,000 (Direct Cost: ¥2,100,000、Indirect Cost: ¥630,000)
Fiscal Year 2015: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2014: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
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| Keywords | ミトコンドリア / 心血管疾患 / 循環器 |
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| 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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Report
(3 results)
Research Products
(11 results)
