2018 Fiscal Year Final Research Report
Molecular mechanism in atheroprotective effects by the enzymes that control membrane sphingolipid levels
| Project/Area Number |
16K15409
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Multi-year Fund |
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| Research Field |
General internal medicine(including psychosomatic medicine)
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| Research Institution | Kanazawa University |
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Principal Investigator |
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| Project Period (FY) |
2016-04-01 – 2019-03-31
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| Keywords | 動脈硬化 / 老年医学 / スフィンゴ脂質代謝 |
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| Outline of Final Research Achievements |
In mice in which the metabolic enzyme was systematically deleted, atherosclerotic lesions were significantly increased by loading with a cholesterol diet. And, it was thought that the enzyme present in bone marrow-derived cells, particularly macrophages, were strongly involved. This enzyme might have atheroprotective role.
After macrophages take up unnecessary or modified lipids, they change to foam cells and deposit in arterial blood vessels followed by blood flow problems. By the analysis of lipid uptake and degradation functions, lipolysis-related autophagic pathways may be mainly impaired in enzyme deleted macrophages.
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| Free Research Field |
内科系臨床医学
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| Academic Significance and Societal Importance of the Research Achievements |
これまでにも全世界で動脈硬化治療薬の開発が行われて来たが、未だ画期的な治療薬は作出されて来なかった。新しい治療薬の開発の為には、新しい観点からの動脈硬化形成機序を明らかにする事が重要である。本研究により、スフィンゴ脂質代謝を制御する鍵酵素が持つ抗動脈硬化作用がオートファジー制御という新しい観点から発揮される事が判明した。これらは今後、新規動脈硬化治療法の開発基盤への有益な情報提供となる。
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