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Calcium-Signalling in Human Glaucoma Lamina Cribrosa Myofibroblasts
Mustapha Irnaten1, Colm J O'Brien1
1Department of Ophthalmology, Mater University Hospital, Eccles Street, D07F851 Dublin, Ireland.
International Journal of Molecular Sciences
|January 21, 2023
Summary
Calcium signaling is abnormal in human glaucoma lamina cribrosa (LC) cells, involving increased calcium entry and release from internal stores. This dysfunction offers potential therapeutic targets for optic neuropathy.
Area of Science:
- Ophthalmology
- Cell Biology
- Biochemistry
Background:
- Glaucoma is a leading cause of irreversible blindness, affecting millions globally.
- Optic nerve damage in glaucoma involves fibrosis in the lamina cribrosa (LC) extracellular matrix.
- Calcium (Ca2+) acts as a critical second messenger in cellular processes and disease.
Purpose of the Study:
- To summarize molecular Ca2+-dependent mechanisms underlying abnormal Ca2+ signaling in human glaucoma LC cells.
- To identify potential therapeutic targets for glaucoma-related optic neuropathy.
Main Methods:
- Analysis of Ca2+ signaling pathways in human glaucomatous LC fibroblast cells.
- Investigating Ca2+ entry channels, pumps, exchangers, and intracellular Ca2+ release mechanisms.
Main Results:
- Evidence of oxidative stress and mitochondrial dysfunction in glaucomatous LC cells.
- Elevated expression of Ca2+ channels, pumps, and exchangers observed.
- Abnormal cytosolic Ca2+ rise dependent on plasma membrane channels and release from ER and mitochondria.
Conclusions:
- Abnormal Ca2+ signaling is a key feature of human glaucoma LC cells.
- Targeting specific Ca2+ signaling pathways may offer novel therapeutic strategies for optic neuropathy.
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