| Project/Area Number |
15K15273
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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 | Osaka University |
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Principal Investigator |
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| Research Collaborator |
NOZATO Satoko 大阪大学, 大学院医学系研究科 老年・総合内科学, 大学院生
TAKESHITA Hikari 大阪大学, 大学院医学系研究科 老年・総合内科学, 特任研究員 (10791577)
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| Project Period (FY) |
2015-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥3,640,000 (Direct Cost: ¥2,800,000、Indirect Cost: ¥840,000)
Fiscal Year 2016: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2015: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Keywords | サルコペニア / レニンーアンジオテンシン系 / ACE2 / 老化 / 骨格筋 / アンジオテンシン |
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| Outline of Final Research Achievements |
Sarcopenia is an aging-related loss of skeletal muscle quantitiy and function, and the treatment of sarcopenia is an emerging strategy of preventing falls in the elderly. In this study, we focused on ACE2 and A1-7 that are components in the renin-angiotensin system, and investigated whether and how these components contribute to the prevention of sarcopenia. Using knockout mice, we found that the deletion of ACE2 exaggerated aging-related skeletal muscle weakness,and A1-7 infusion improved skeletal muscle function in aged mice. These findings were acompanied by up-regulation of p16, a senescence-associated gene in ACE2 knockout mice. Using mice deleted for Mas,a known receptor of A1-7,we also found the results supporting the notion that ACE2-A1-7 improves aging-associated skeletal muscle weakness via both Mas dependent and indepent pathway.
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