Publications by authors named "Emma K Geiduschek"
DAMPs Drive Fibroinflammatory Changes in the Glaucomatous ONH.
Invest Ophthalmol Vis Sci
October 2024
Article Synopsis
- - The study investigates the early molecular mechanisms behind glaucoma, focusing on B6.EDA+/+ mice, which express a damage-associated molecule (FN+EDA) that triggers an inflammatory response in the optic nerve head.
- - Researchers found that these mice experience significantly higher intraocular pressure and retinal damage compared to control mice, with increased expression of proteins like FN+EDA and biglycan linked to these changes.
- - Gene analysis and protein expression studies over two years revealed new molecular pathways related to glaucomatous damage, highlighting the role of FN+EDA in promoting inflammation in the optic nerve head as the mice aged.
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.
View Article and Find Full Text PDFTLR4 signaling modulates extracellular matrix production in the lamina cribrosa.
Front Ophthalmol (Lausanne)
August 2022
The optic nerve head (ONH) is a place of vulnerability during glaucoma progression due to increased intraocular pressure damaging the retinal ganglion cell axons. The molecular signaling pathways involved in generating glaucomatous ONH damage has not been fully elucidated. There is a great deal of evidence that pro-fibrotic TGFβ2 signaling is involved in modulating the ECM environment within the lamina cribrosa (LC) region of the ONH.
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