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2023 Fiscal Year Final Research Report

Functional analysis of novel non-coding RNAs in age related macular degeneration

Research Project

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Project/Area Number 20K09821
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeMulti-year Fund
Section一般
Review Section Basic Section 56060:Ophthalmology-related
Research InstitutionYokohama City University

Principal Investigator

YANAGI Yasuo  横浜市立大学, 医学研究科, 客員教授 (90376442)

Co-Investigator(Kenkyū-buntansha) 藤生 克仁  東京大学, 医学部附属病院, 特任准教授 (30422306)
Project Period (FY) 2020-04-01 – 2023-03-31
Keywords加齢黄斑変性
Outline of Final Research Achievements

This study identified non-coding RNAs (ncRNAs) and long non-coding RNAs (lncRNAs) as novel targets for age-related macular degeneration (AMD) using bioinformatics and clinical sample analysis. We tested the therapeutic potential of a miRNA mimic targeting "Target A" in AMD mouse models. Fluorescence fundus angiography showed a significant reduction in CNV fluorescence leakage in the "Target A" group compared to controls, and choroidal flat-mounts showed significant CNV size suppression. In VLDLR knockout mice, "Target A" reduced endothelial markers PECAM-1, VEGFR1, and VEGFR2, but not VEGF-A. These findings suggest "Target A" miRNA mimic could inhibit CNV in AMD, highlighting its potential as a therapeutic candidate. Further research on ncRNAs and lncRNAs in AMD is crucial for developing new treatments.

Free Research Field

眼科

Academic Significance and Societal Importance of the Research Achievements

本研究は加齢黄斑変性における新たな治療ターゲットとして、ノンコーディングRNA(ncRNA)およびロングノンコーディングRNA(lncRNA)の役割を明らかにした。学術的には、AMDにおけるこれらncRNAの具体的な機能を初めて示し、特に"標的A"のmiRNA mimicが脈絡膜新生血管(CNV)の抑制に寄与することを発見した。これにより、AMD治療の新たな分子メカニズムが解明され、基礎研究と臨床研究において重要な進展が期待される。社会的には、既存治療に加え新規治療法の開発が患者の治療選択肢を拡げる可能性がある。

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Published: 2025-01-30  

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