2019 Fiscal Year Final Research Report
Mechanism of sarcopenia based on analysis of Werner syndrome
Project/Area Number |
17K09292
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Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
General internal medicine(including psychosomatic medicine)
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Research Institution | Chiba University |
Principal Investigator |
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Co-Investigator(Kenkyū-buntansha) |
竹本 稔 千葉大学, 大学院医学研究院, 特任教授 (60447307)
前澤 善朗 千葉大学, 大学院医学研究院, 講師 (80436443)
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Project Period (FY) |
2017-04-01 – 2020-03-31
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Keywords | 早老症 / サルコペニア / iPS細胞 |
Outline of Final Research Achievements |
Werner's syndrome (hereinafter, WS) is a hereditary progeria that prematurely causes aging signs such as gray hair, hair loss, cataracts and skin atrophy, diabetes and arteriosclerosis, and causes myocardial infarction and cancer after the age of 30. Since WS patients often exhibit strong sarcopenia, this study elucidated the mechanism of sarcopenia in WS patients. We established adipose tissue mesenchymal stem cells directly collected from WS patients. In addition, we established WS disease-specific iPS cells, and attempted to induce differentiation into mesenchymal stem cells. Then, it was found that WS-derived mesenchymal stem cells and WS-iPSC-derived mesenchymal stem cells exhibited signs of early senescence. In addition, differentiation into muscle cells is planned in the future.
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Free Research Field |
老化、糖尿病
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Academic Significance and Societal Importance of the Research Achievements |
サルコペニアは高齢者において転倒骨折、寝たきりやQOL低下の強いリスクである。本研究はヒト早老症の解析からヒトのサルコペニアの病態解明や治療開発に役立つ知見を得たいと考えており、サルコペニアの新たな治療戦略や治療薬開発への基盤となることが期待される。
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