| Project/Area Number |
25460397
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Pathological medical chemistry
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| Research Institution | Osaka Medical College |
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Principal Investigator |
Asahi Michio 大阪医科大学, 医学部, 教授 (10397614)
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| Co-Investigator(Kenkyū-buntansha) |
中山 博之 大阪大学, 薬学研究科, 准教授 (40581062)
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| Co-Investigator(Renkei-kenkyūsha) |
Azuma Naoto 大阪医科大学, 医学部, 教授 (40231914)
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| Research Collaborator |
Ii Masaaki
Nakagawa Takatoshi
Moriwaki Kazumasa
Ai Tomohiko
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| Project Period (FY) |
2013-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥5,200,000 (Direct Cost: ¥4,000,000、Indirect Cost: ¥1,200,000)
Fiscal Year 2015: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2014: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2013: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Keywords | O-GlcNAc修飾 / O-GlcNAc転移酵素 / 大動脈縮窄術 / NFAT / GSK3β / ホスホランバン / STIM-1 / 糖鎖 / 心筋小胞体タンパク質 |
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| Outline of Final Research Achievements |
The cardiac function in diabetic patients is often reduced, although coronary areteries are intact. Metabolic abnormality of cardiac muscle might be involved in the etiology, and the pathologic condition is named diabetic cardiomyopathy. However, the mechanism was not fully understood. In this study, we focused on O-GlcNAcylation which was augmented in diabetes, and examined how the modification affected the cardiac function. As a result, we found that some proteins related to cardiac function were inactivated by O-GlcNAcylation. The downregulation of cardiac function by O-GlcNAcylation might be one of the cause of diabetic cardiomyopathy. In the future, based on this basic research, I would like to connect it with new drug development.
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