Mitochondrial dysfunction on acute myocardial infarction or MDMA poisoning
| Project/Area Number |
25293162
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Partial Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Legal medicine
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| Research Institution | Kyoto Prefectural University of Medicine (2014-2015)
The University of Tokyo (2013) |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
INUI Makoto 山口大学, 大学院医学系研究科, 教授 (70223237)
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| Project Period (FY) |
2013-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥17,940,000 (Direct Cost: ¥13,800,000、Indirect Cost: ¥4,140,000)
Fiscal Year 2015: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2014: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2013: ¥14,690,000 (Direct Cost: ¥11,300,000、Indirect Cost: ¥3,390,000)
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| Keywords | 急性心筋梗塞 / ＭＤＭＡ / ミトコンドリア / カルパイン / オートファジー / MDMA / セロトニン / 心臓突然死 / 心筋梗塞 |
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| Outline of Final Research Achievements |
The aims of this study was to clarify the molecular mechanisms of cardiac dysfunction, especially of mitochondria dysfunction, on acute myocardial infarction or a designer drug MDMA poisoning, and new findings were as follow;
1. Mitochondria of both rat and human cardiomyocytes have a calcium-dependent protease caplain. Acute myocardial infarction-activated mitochondrial calpain cleaves mitochondrial functional proteins, resulting in cardiac dysfunction.
2. In rat heart, MDMA causes lysosome destabilization following activation of the autophagy-lysosomal pathway, through which released lysosomal proteases damage myofibrils and induce cardiac dysfunction.
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Report
(4 results)
Research Products
(18 results)
