Preprint Review Version 1 Preserved in Portico This version is not peer-reviewed

AIBP: A New Safeguard against Glaucomatous Neuroinflammation

Seunghwan Choi
,
Soo-Ho Choi
* ORCID logo ,
Tonking Bastola
,
Young Gun Park
,
Jonghyun Oh
,
Keun-Young Kim
,
Sinwoo Hwang
ORCID logo ,
Yury I. Miller
,
Won-Kyu Ju
* ORCID logo
Version 1 : Received: 14 December 2023 / Approved: 14 December 2023 / Online: 14 December 2023 (14:00:38 CET)

A peer-reviewed article of this Preprint also exists.

Choi, S.; Choi, S.-H.; Bastola, T.; Park, Y.; Oh, J.; Kim, K.-Y.; Hwang, S.; Miller, Y.I.; Ju, W.-K. AIBP: A New Safeguard against Glaucomatous Neuroinflammation. Cells 2024, 13, 198. Choi, S.; Choi, S.-H.; Bastola, T.; Park, Y.; Oh, J.; Kim, K.-Y.; Hwang, S.; Miller, Y.I.; Ju, W.-K. AIBP: A New Safeguard against Glaucomatous Neuroinflammation. Cells 2024, 13, 198.

Abstract

Glaucoma is a group of ocular diseases that causes irreversible blindness worldwide and is characterized by a multifactorial degeneration of optic nerve and retinal ganglion cells (RGCs), leading to vision loss. One of the significant risk factors in glaucoma pathogenesis is glia-driven neuroinflammation. Impairment of mitochondrial dynamics and bioenergetics is associated with glaucomatous neurodegeneration and is linked to neuroinflammation. Apolipoprotein A-I binding protein (AIBP) binds to toll-like receptor 4 (TLR4) and facilitates the removal of excess cholesterol from the plasma membrane in activated cells, suggesting the regulation of cholesterol-driven inflammation by inhibiting the TLR4-associated lipid rafts. AIBP is localized in mitochondria and regulates mitophagy by ubiquitination of mitofusin 1 and 2. We observed elevated intraocular pressure-induced AIBP deficiency in glaucomatous neurodegeneration. We also observed that AIBP deficiency activated TLR4 in Müller glia, triggered mitochondrial dysfunction in both RGCs and Müller glia and impaired visual function. In mouse models of glaucoma, AIBP treatment protects RGCs by reducing inflammatory responses. Here, our review focuses on investigating the role of AIBP in the retina and examining the underlying mechanism by which AIBP contributes to the pathogenesis of glaucoma, aiming to provide new insight into the therapeutic potential for the treatment of glaucoma.

Keywords

AIBP; Glaucoma; Neuroinflammation; Cholesterol; TLR4; Lipid rafts; Mitochondria; Gene therapy; AAV

Subject

Biology and Life Sciences, Neuroscience and Neurology

Copyright: This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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