| Project/Area Number |
18K15014
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| Research Category |
Grant-in-Aid for Early-Career Scientists
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| Allocation Type | Multi-year Fund |
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| Review Section |
Basic Section 48020:Physiology-related
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| Research Institution | Kitasato University |
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Principal Investigator |
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| Project Period (FY) |
2018-04-01 – 2020-03-31
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| Project Status |
Completed (Fiscal Year 2019)
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| Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2019: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2018: ¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
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| Keywords | 虚血再灌流 / 再酸素化 / 心筋細胞 / 心臓 / コンディショニング |
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| Outline of Final Research Achievements |
I previously reported a novel protein SSKH1, which is drastically upregulated in cardiomyocytes in response to ischemia reperfusion or reoxygenation after hypoxia. In this study, various organs in mice were subjected to ischemia reperfusion injury, and in consequence, the dramatic upregulation of SSKH1 was found to be unique to hearts. Sskh1 deficiency reduced myocardial infarct size after ex vivo or in vivo ischemia/reperfusion injury. However, the mortality rate after ischemia reperfusion injury was significantly higher in Sskh1 knockout mice compared with wild-type mice. Pulmonary congestion during reperfusion, resulting from low cardiac output, was more frequently observed in Sskh1 knockout mice. These results suggest that SSKH1 does not protect cardiomyocyte injury but it protects cardiac electrophysiological activity.
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| Academic Significance and Societal Importance of the Research Achievements |
再灌流障害は出血やショック、虚血性心疾患、心血管の外科的手術、臓器移植などで認められる、臨床上、重大な合併症である。再酸素化により細胞障害が誘起される一方、障害に対する保護作用も同時に亢進している。この保護作用はコンディショニングという現象で実証され、様々な作用機序が提唱されている。現在までに、それら保護作用を間欠的虚血処置や薬剤などで活性化して再灌流障害の予防や治療に臨床応用する研究が盛んに行われている。本研究成果はそれら保護作用の一つを説明するものであり、コンディショニング研究の一助となる。
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