TBK1 Knockdown Alleviates Axonal Transport Deficits in Retinal Ganglion Cells Via mTORC1 Activation in a Retinal Damage Mouse Model.

ABSTRACT:

Purpose

Glaucoma is the leading cause of irreversible blindness worldwide and is characterized by progressive retinal ganglion cell (RGC) death and optic nerve degeneration. Axonal transport deficits are the earliest crucial pathophysiological changes in glaucoma. Genetic variation in the TANK-binding kinase 1 gene (TBK1) plays a role in the pathogenesis of glaucoma. This study was designed to investigate intrinsic factors underlying RGCs' damage and to explore the molecular mechanism of TBK1 involvement in glaucomatous pathogenesis.

Methods

We established a mouse model of acute ocular hypertension and used TBK1 conditional knockdown mice to investigate the role of TBK1 in glaucoma. CTB-Alexa 555 was utilized to evaluate axonal transport in mice. To observe the efficiency of

SUBMITTER: Ye M 

PROVIDER: S-EPMC10324417 | biostudies-literature | 2023 Jul

REPOSITORIES: biostudies-literature