| Project/Area Number |
26293186
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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 |
Cardiovascular medicine
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| Research Institution | Kyoto University |
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Principal Investigator |
Ono Koh 京都大学, 医学(系)研究科(研究院), 准教授 (00359275)
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| Co-Investigator(Kenkyū-buntansha) |
堀江 貴裕 京都大学, 医学(系)研究科(研究院), 助教 (20565577)
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| Co-Investigator(Renkei-kenkyūsha) |
NAKAMURA Tomoyuki 関西医科大学, 薬理学, 教授 (20362527)
MARUSAWA Hiroyuki 京都大学, 大学院医学研究科, 准教授 (80324630)
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| Project Period (FY) |
2014-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥16,770,000 (Direct Cost: ¥12,900,000、Indirect Cost: ¥3,870,000)
Fiscal Year 2016: ¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000)
Fiscal Year 2015: ¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000)
Fiscal Year 2014: ¥7,930,000 (Direct Cost: ¥6,100,000、Indirect Cost: ¥1,830,000)
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| Keywords | マイクロRNA / 動脈硬化 / 線維化 / ナノ粒子 / HDL-C / 炎症 / コレステロール / 慢性炎症 / 骨髄 |
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| Outline of Final Research Achievements |
MicroRNAs (miRNAs; miRs) are small non-protein-coding RNAs that negatively regulate gene expression. They bind to the 3’UTR of specific mRNAs and inhibit translation or promote mRNA degradation. There is emerging evidence linking miR-33a/b to lipid homoeostasis, targeting ABCA1, SREBF1, etc. Such functions of miR-33a/b appear to serve as “thrifty genes” during evolution to maintain cholesterol levels both at cellular and whole body levels. As we are now living in a “satiation period,” miR-33a/b no longer seem to be useful and could be potential therapeutic targets for lipid disorders and/or atherosclerosis. In fact, we have found that existence of miR-33a/b can lead to the occurrence of atherosclerosis, chronic inflammation, and cardiac fibrosis in vivo. Fine regulation of miR-33a/b could be a promising new approach for the prevention or treatment of cardiovascular diseases in the future.
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