Mechanism of TBK1 in Glaucoma by Regulating Retinal Ganglion Apoptosis

Lijun Ren, Xuemei Pu, Chong Gao and Juan Yu

Background and Objective: Glaucoma is a leading cause of irreversible blindness worldwide. Despite its prevalence, the specific mechanisms underlying retinal ganglion cell (RGC) injury remain unclear, posing a significant challenge in reducing RGC apoptosis in glaucoma patients. This study aimed to investigate the regulatory effect of TBK1 on retinal ganglion apoptosis and its related mechanism. Materials and Methods: Fifty healthy male adult SD rats were randomly divided into control group (Sham group), optic nerve contusion group (VD group), TBK1 overexpression lentivirus vector+optic nerve contusion group (VD+TBK1 group), lentivirus vector+optic nerve contusion group (VD+VS group) and TBK1 inhibitor BX795+optic nerve contusion group (VD+B group), with 10 rats in each group. Results: Compared to Sham group, the eye histopathology worsened in VD, VD+VS and VD+B groups, with increased serum levels of IL-1β, IL-6 and TNF-α, decreased TBK1 protein expression and increased RIPK1 and caspase-3 protein expression. Compared to Sham group, the eye histopathology deteriorated in VD+TBK1 group, with increased IL-1β, IL-6 and TNF-α and increased TBK1, RIPK1 and caspase-3 protein expression. Compared to VD group, the eye histopathology worsened in VD+B group, with elevated IL-1β, IL-6 and TNF-α, decreased TBK1 protein expression and increased RIPK1 and caspase-3 protein expression. Compared to VD group, the eye histopathology showed improvement in VD+TBK1 group, with decreased IL-1β, IL-6 and TNF-α, increased TBK1 protein expression and decreased RIPK1 and caspase-3 protein expression. Conclusion: The TBK1 regulates inflammatory factors TNF-α, IL-6, IL-1β, inhibits RIPK1 and caspase protein expression and regulates the apoptosis of retinal ganglion in glaucoma.

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