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2019 Fiscal Year Final Research Report

The mechanism of age-related macular degeneration by measuring intraocular complement factors and related proteins

Research Project

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Project/Area Number 17K11427
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeMulti-year Fund
Section一般
Research Field Ophthalmology
Research InstitutionFukushima Medical University

Principal Investigator

Tetsuju Sekiryu  福島県立医科大学, 医学部, 教授 (00216540)

Co-Investigator(Kenkyū-buntansha) 関根 英治  福島県立医科大学, 医学部, 教授 (40363759)
大口 泰治  福島県立医科大学, 医学部, 助教 (90595331)
小島 彰  福島県立医科大学, 医学部, 助教 (30528237)
菅野 幸紀  福島県立医科大学, 医学部, 助教 (40644828)
Project Period (FY) 2017-04-01 – 2020-03-31
Keywords滲出型加齢黄斑変性 / 補体 / アナフィラトキシン / サイトカイン / VEGF / MCP-1 / Pachychoroid
Outline of Final Research Achievements

To investigate the effect of intraocular complement factors on angiogenic cytokines in neovascular age-related macular degeneration, we measured anaphylatoxin (C3a, C4a, C5a) concentrations and VEGF, MCP-1 in the aqueous humor.
In neovascular age-related macular degeneration, the concentration of C3a, VEGF, and MCP-1 elevated. The concentration of C3a highly correlated to that of the MCP-1. In contrast, the correlation between the VEGF level and C3a level was low in patchychoroid neovasculopathy. The pathophysiology of pachychoroid neovasculopathy, which is characterized by choroidal thickening, may be different from that of typical neovascular age-related macular degeneration, which is characterized by soft drusen.

Free Research Field

黄斑、網膜硝子体

Academic Significance and Societal Importance of the Research Achievements

滲出型加齢黄斑変性における脈絡膜新生血管の形成には補体因子が関与していることが指摘されていた。今回の研究で、脈絡膜新生血管が補体因子を介さない発症機序で形成されることを前房内蛋白を解析することで生物学的に解明することができた。今後は、従来と異なる脈絡膜新生血管機序を明らかにすることで、新たな滲出型加齢黄斑変性の治療法の開発に結びつけることができると考えている。

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Published: 2021-02-19  

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