Ferroptosis Contributes to Retinal Ganglion Cell Loss in GLAST Knockout Mouse Model of Normal Tension Glaucoma.

ABSTRACT:

Purpose

Visual impairment from normal-tension glaucoma (NTG) poses an increasing burden, yet the underlying mechanism remains unclear. Investigating protective mechanisms for NTG is critical. We aimed to investigate the role of ferroptosis in retinal ganglion cell (RGC) damage in glutamate-aspartate transporter (GLAST) knockout (GLAST-/-) mice, a model for NTG, and also to determine whether inhibiting ferroptosis can provide neuroprotection.

Methods

GLAST-/- mice and a glutamate-induced excitotoxicity model in primary RGCs were used to investigate retinal and RGC damage. RNA sequencing identified ferroptosis-related pathways in GLAST-/- retinas. Oxidative stress, lipid peroxidation, and ferroptosis activation were assessed using western blotting and immunofluorescence. Immun

SUBMITTER: Ye H 

PROVIDER: S-EPMC12110597 | biostudies-literature | 2025 May

REPOSITORIES: biostudies-literature