Mitochondrial damage mediated by pressure gradient in glaucomatous optic neuropathy.

2023 Fiscal Year Final Research Report

• Project/Area Number: 20H03840
• Research Category: Grant-in-Aid for Scientific Research (B)
• Allocation Type: Single-year Grants
• Section: 一般
• Review Section: Basic Section 56060:Ophthalmology-related
• Research Institution: University of Fukui
• Principal Investigator: Inatani Masaru 福井大学, 学術研究院医学系部門, 教授 (40335245)
• Co-Investigator(Kenkyū-buntansha): 高村 佳弘 福井大学, 学術研究院医学系部門, 准教授 (00283193) ; 有村 尚悟 福井大学, 学術研究院医学系部門(附属病院部), 助教 (20835029) ; 辻 隆宏 福井大学, 学術研究院医学系部門(附属病院部), 助教 (40787389)
• Project Period (FY): 2020-04-01 – 2024-03-31
• Keywords: 緑内障

Outline of Final Research Achievements

We used mice without lamina cribrosa to investigate the mechanism of optic nerve damage in glaucoma, observing the dynamics of mitochondria within retinal ganglion cell axons and changes in intracellular ATP gradients. Creating a glaucoma model, we observed an increase in mitochondrial distribution within the axons of retinal ganglion cells and a decrease in axonal movement. These findings suggest a potential impact on mitochondrial dynamics within neurons even in animals without lamina cribrosa. Concurrently, we observed mitochondrial stoppage within axons, accompanied by changes in intracellular ATP gradients. Specifically, changes in mitochondrial dynamics were thought to affect ATP supply within axons, potentially playing a crucial role in cell function and survival.

Free Research Field

緑内障

Academic Significance and Societal Importance of the Research Achievements

この研究から、緑内障視神経症における篩状板の役割に新しい概念をもたらすことができた。さらに、網膜神経節細胞の機能維持におけるミトコンドリアの役割と、網膜神経節細胞の細胞死の過程におけるミトコンドリアとATP勾配の役割を明らかにすることができた。本研究結果は、将来におけるヒトの緑内障の視神経障害の診断や治療に役立つ情報を提供できる可能性がある。