IL-6 as a target for delay the progression of muscular dystrophy
| Project/Area Number |
16K18385
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Nerve anatomy/Neuropathology
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| Research Institution | Tokyo Medical University |
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Principal Investigator |
WADA EIJI 東京医科大学, 医学部, 助教 (60756948)
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| Project Period (FY) |
2016-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥2,600,000 (Direct Cost: ¥2,000,000、Indirect Cost: ¥600,000)
Fiscal Year 2017: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2016: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
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| Keywords | デュシェンヌ型筋ジストロフィー / 筋疾患 / IL-6 / 線維化 / 筋再生 / 筋衛星細胞 / 炎症 / 筋ジストロフィー / 骨格筋 / インターロイキン6 / 骨格筋の線維化 / 骨格筋幹細胞 / 神経科学 |
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| Outline of Final Research Achievements |
Interleukin-6 (IL-6) is related to inflammation and fibrosis but is also known as a myokine in skeletal muscle. Elevated IL-6 levels in blood and skeletal muscle are observed in patients and model animals of Duchenne muscular dystrophy (DMD); however, its contribution to the progression of muscular dystrophy is unclear. This study aimed to evaluate the effects of IL-6 receptor (IL-6R) blockage on the muscle pathology in DMD model mice. Treatment of IL-6R blockage successfully inhibited IL-6 pathway in skeletal muscle and significantly increased regenerating fibers. A significant reduction of phosphorylated STAT3 in skeletal muscle of treated mice supported the effects of IL-6R blockage on promoting muscle regeneration. Consistently, decreased serum CK levels, enlarged muscle diameter and reduced fibrosis in quadriceps muscle were seen. These results indicate that anti IL-6R antibody is a potential therapy for dystrophic muscle particularly for activating skeletal muscle regeneration.
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Report
(3 results)
Research Products
(7 results)
