2022 Fiscal Year Final Research Report
The complement lectin pathway is involved in the development of exudative age-related macular degeneration
Project/Area Number |
20K09776
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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 |
Review Section |
Basic Section 56060:Ophthalmology-related
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Research Institution | Fukushima Medical University |
Principal Investigator |
Omori Tomoko 福島県立医科大学, 医学部, 助教 (50754222)
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Co-Investigator(Kenkyū-buntansha) |
石龍 鉄樹 福島県立医科大学, 医学部, 教授 (00216540)
関根 英治 福島県立医科大学, 医学部, 教授 (40363759)
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Project Period (FY) |
2020-04-01 – 2023-03-31
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Keywords | 補体 |
Outline of Final Research Achievements |
This study was aimed at clarifying the involvement of lectin pathway activation in the development of age-related macular degeneration (AMD). We used MASP-1-deficient mice, which lack lectin pathway activity, and injected NaIO3 into these mice to analyze pathology of retina degeneration. Retinal degeneration was mild in NaIO3-injected MASP-1 mice compared with NaIO3-injected wild type mice. On the other hand, C3 activation levels did not differ between NaIO3-injected MASP-1 and NaIO3-injected wild type mice. This study suggests that MASP-1 is one of the exacerbating factors in the development of AMD. Further study is needed to clarify involvement of the lectin pathway activation in the development of AMD.
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Free Research Field |
免疫学
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Academic Significance and Societal Importance of the Research Achievements |
本研究の結果、加齢黄斑変性のモデルであるヨウ素酸ナトリウム誘発網膜障害モデルにおける網膜障害にMASP-1が増悪因子として作用することが示唆された。この成果は、加齢黄斑変性の病態における補体の関与への理解を深め、加齢黄斑変の新規治療法の開発につながると期待される。
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