Investigation of the mechanism of ischemic re-perfusion injury after myocardial infarction
| Project/Area Number |
25861714
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Emergency medicine
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| Research Institution | University of Tsukuba |
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Principal Investigator |
KIMURA Taizo 筑波大学, 附属病院, 病院講師 (00636508)
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| Project Period (FY) |
2013-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2014: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2013: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | テネイシンC / 心筋梗塞 / 心室リモデリング / 虚血再還流傷害 |
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| Outline of Final Research Achievements |
Left ventricular remodeling following myocardial infarction (MI) is a major cause of heart failure and have high concordance with long-term clinical outcomes. Thus, to investigate the mechanism of left ventricular remodeling after MI and prevent it is one of the important clinical issues.
In this study, we showed that an extracellular matrix glycoprotein, Tenascin-C (TN-C) Knock-out mice had the better cardiac function than Wild type (WT) mice at chronic phase after myocardial infarction. And at acute phase after myocardial infarction, we showed that ratio of pro-inflammatory macrophage was significantly decreased and anti-inflammatory macrophage was significantly decreased in myocardial tissue of TN-C knock-out mice compared with WT mice.
These findings suggest,TN-C aggravates the deterioration of LV function due to Myocardial infarction in chronic phase partly through the promotion of inflammation at acute phase.
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Report
(3 results)
Research Products
(3 results)
