2018 Fiscal Year Final Research Report
Biological mechanism of novel sarcopenia related microRNA
| Project/Area Number |
17H07012
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| Research Category |
Grant-in-Aid for Research Activity Start-up
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| Allocation Type | Single-year Grants |
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| Research Field |
Laboratory medicine
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| Research Institution | Kyoto Prefectural University of Medicine |
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Principal Investigator |
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| Project Period (FY) |
2017-08-25 – 2019-03-31
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| Keywords | サルコペニア / microRNA / 筋肉 |
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| Outline of Final Research Achievements |
Although sarcopenia is known as a risk factor for quality of life decline and shortened life expectancy, there are currently no effective treatments and no bio-markers for sarcopenia. We focus on the role of microRNA on saropenia and previously revealed that mir-23 is increasing in muscle with muscle atrophy. Thus, we hypothesis that mir-23 has a role on sarcopenia.
In this study, we examined the impact and the mechanisms of mir-23 on saropenia. We revealed that mir-23b was increased through muscle atrophy in the mouse model. In addition, we clarified that mir-23b acts as protectively on muscle atrophy through suppressing Phosphatase and Tensin Homolog Deleted from Chromosome and enhancing Akt-mTOR pathway. Furthermore, we showed that serums of mir-23a and mir-23b in people with sarcopenia were higher than those in people without sarcopenia.
These results suggest that mir-23 might be a novel therapeutic target and diagnostic biomarker for sarcopenia.
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| Free Research Field |
内分泌・代謝
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| Academic Significance and Societal Importance of the Research Achievements |
サルコペニア（筋萎縮）はQOLおよび生命予後を著しく低下させるが、現在有効な治療はなく、サルコペニアの早期診断や発症予測となるバイオマーカーもない。
本研究では申請者らが発見した筋委縮関連microRNAであるmir-23が筋委縮に対して防護的に働いていることおよび実際サルコペニアを呈する人血清ではmir-23が増加していることを明らかにした。これらの結果からmir23はサルコペニアの新規の治療ターゲットとなりうる可能性および早期診断のバイオマーカーになりうる可能性がある。
今後、mir23を用いて、サルコペニア予防とそれに伴うQOLおよび生命予後の改善を目指す一助になる。
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