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The Fibro-Inflammatory Response in the Glaucomatous Optic Nerve Head

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MDPI
DOI: 10.3390/ijms241713240

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glaucoma; TLR4; fibrosis; immune response; optic nerve head; TGF beta 2

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Glaucoma is a progressive disease that leads to irreversible blindness. Understanding the cellular mechanisms behind optic nerve head damage during disease progression can help identify new drug targets and therapeutic strategies.
Glaucoma is a progressive disease and the leading cause of irreversible blindness. The limited therapeutics available are only able to manage the common risk factor of glaucoma, elevated intraocular pressure (IOP), indicating a great need for understanding the cellular mechanisms behind optic nerve head (ONH) damage during disease progression. Here we review the known inflammatory and fibrotic changes occurring in the ONH. In addition, we describe a novel mechanism of toll-like receptor 4 (TLR4) and transforming growth factor beta-2 (TGF beta 2) signaling crosstalk in the cells of the ONH that contribute to glaucomatous damage. Understanding molecular signaling within and between the cells of the ONH can help identify new drug targets and therapeutics.

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