2020 Fiscal Year Final Research Report
Mechanism in photoreceptor cell death
| Project/Area Number |
17K11448
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Ophthalmology
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| Research Institution | Osaka University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
松下 賢治 大阪大学, 医学系研究科, 講師 (40437405)
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| Project Period (FY) |
2017-04-01 – 2021-03-31
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| Keywords | 視細胞死 / 加齢黄斑変性 / 網膜色素変性 |
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| Outline of Final Research Achievements |
We have researched pathology in ophthalmologic field sing zebrafish model in reverse genetics. In this study, we have mainly analyzed a role of HTRA1, which is a strong disease related gene in age-related macular degeneration. HTRA1 induction in photoreceptors resulted in photoreceptor cell death. The expression of HTRA1 is induced by age and the mutation. The downstream of HTRA1 related to TGF beta - FOXO signal. We have also researched Eys gene function, which is a main cause of Japanese retinaitis pigmentosa.
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| Free Research Field |
病態学
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| Academic Significance and Societal Importance of the Research Achievements |
加齢黄斑変性の治療は現在のところ、血管新生因子に対する介入療法である。しかし、これは病態の最終段階への介入であり、効果は限られる。今回疾患感受性遺伝子変異であるHTRA1の発現亢進が視細胞死を引き起こし、それが加齢黄斑変性の発症につながるという新たな発症機序が明らかになったことで、新たな治療戦略がとれるようになり、実際に製薬企業との共同研究につながった。また、学術的にも新たな病因論を提案したため、その価値は高い。
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