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. 2022 Sep 25;12(10):1368. doi: 10.3390/biom12101368

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© 2022 by the authors.

Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/).

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Normal retina and optic nerve head (ONH) (A). Retinal ganglion cell (RGC) axon bundle passes lamina cribrosa (LC) and exits the eye. LC supports the RGC axon bundles as they become the optic nerve. Glaucomatous ONH change (B). Increased intraocular pressure causes mechanical stress in the LC. Due to mechanical stress in LC, cytokine activity is increased, which induces matrix metalloproteinase (MMP) expression and extracellular matrix (ECM) remodeling in the ONH. Additionally, mechanical stress cause apoptosis of RGC by increased MMP-9 activity. The aftermath of glaucomatous ONH changes includes cupping of ONH (yellow arrows), retinal nerve fiber layer thinning by RGC apoptosis (red double arrow), and lamina cribrosa disruption (blue arrows) [31,95,96,97,98].