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REVIEW article

Front. Neurosci.

Sec. Neurodegeneration

Tank-Binding Kinase 1 Regulates Inflammation and Autophagy in Glaucoma

Provisionally accepted
Autumn  B. MorganAutumn B. Morgan1,2Denise  M InmanDenise M Inman1,2*
  • 1Department of Pharmaceutical Sciences, University of North Texas Health Science Center, Fort Worth, Texas, United States
  • 2University of North Texas Health Science Center at Fort Worth North Texas Eye Research Institute, Fort Worth, United States

The final, formatted version of the article will be published soon.

TANK-binding kinase (TBK1) copy number variations have been identified as a monogenic cause of familial normal tension glaucoma (NTG). While elevated intraocular pressure (IOP) is a common risk factor in primary open angle glaucoma (POAG), NTG develops in the absence of IOP elevation. The current available standard of care for glaucoma is lowering IOP, highlighting the need to explore alternative therapeutic mechanisms. The established roles of TBK1 in nuclear factor kappa B (NF-kB) and interferon regulatory factor (IRF) signaling, as well as its involvement in autophagy, suggest it may contribute to glaucomatous neurodegeneration by exacerbating retinal ganglion cell (RGC) stress and optic nerve (ON) damage. This review aims to consolidate current knowledge on the contribution of TBK1 to glaucomatous pathology, focusing on its genetic and molecular roles. By identifying gaps in understanding, this work seeks to guide future research efforts into the mechanisms underlying TBK1's influence on NTG and to explore therapeutic strategies targeting its pathways.

Keywords: mitophagy, NF-kB, Normal tension glaucoma, optic neuropathy, TNFa

Received: 30 Oct 2025; Accepted: 04 Dec 2025.

Copyright: © 2025 Morgan and Inman. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

* Correspondence: Denise M Inman

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