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The role of epigenetics in the fibrotic processes associated with glaucoma
Fiona McDonnell1, Colm O'Brien2, Deborah Wallace2
1UCD School of Medicine and Medical Science, University College Dublin, Dublin, Ireland.
Abstract:
Glaucoma is an optic neuropathy that affects 60 million people worldwide. The main risk factor for glaucoma is increased intraocular pressure (IOP), this is currently the only target for treatment of glaucoma. However, some patients show disease progression despite well-controlled IOP. Another possible therapeutic target is the extracellular matrix (ECM) changes in glaucoma. There is an accumulation of ECM in the lamina cribrosa (LC) and trabecular meshwork (TM) and upregulation of profibrotic factors such as transforming growth factor β (TGF β ), collagen1 α 1 (COL1A1), and α -smooth muscle actin ( α SMA). One method of regulating fibrosis is through epigenetics; the study of heritable changes in gene function caused by mechanisms other than changes in the underlying DNA sequence. Epigenetic mechanisms have been shown to drive renal and pulmonary fibrosis by upregulating profibrotic factors. Hypoxia alters epigenetic mechanisms through regulating the cell's response and there is a hypoxic environment in the LC and TM in glaucoma. This review looks at the role that hypoxia plays in inducing aberrant epigenetic mechanisms and the role these mechanisms play in inducing fibrosis. Evidence suggests that a hypoxic environment in glaucoma may induce aberrant epigenetic mechanisms that contribute to disease fibrosis. These may prove to be relevant therapeutic targets in glaucoma.
Insights
Glaucoma patients may progress despite controlled eye pressure. Hypoxia in the optic nerve may trigger epigenetic changes, leading to fibrosis and disease progression, offering new therapeutic targets.
Area of Science:
- Ophthalmology
- Molecular Biology
- Epigenetics
Background:
- Glaucoma affects 60 million globally, with elevated intraocular pressure (IOP) as the primary risk factor.
- Disease progression occurs even with controlled IOP, suggesting alternative therapeutic targets.
- Extracellular matrix (ECM) accumulation and profibrotic factor upregulation are observed in glaucoma's lamina cribrosa (LC) and trabecular meshwork (TM).
Purpose of the Study:
- To review the role of hypoxia in inducing aberrant epigenetic mechanisms in glaucoma.
- To explore how these epigenetic changes contribute to fibrosis in the optic nerve.
- To identify potential new therapeutic targets for glaucoma treatment.
Main Methods:
- Literature review focusing on the interplay between hypoxia, epigenetics, and fibrosis in glaucoma.
- Analysis of studies investigating epigenetic modifications in the context of profibrotic factor regulation.
- Examination of the hypoxic environment within the LC and TM in glaucoma patients.
Main Results:
- Hypoxia is present in the LC and TM of glaucomatous eyes.
- Aberrant epigenetic mechanisms are implicated in driving fibrosis by upregulating profibrotic factors.
- These hypoxia-induced epigenetic changes may contribute to ECM accumulation in glaucoma.
Conclusions:
- A hypoxic environment in glaucoma may induce epigenetic alterations that promote fibrosis.
- Epigenetic mechanisms represent a potential therapeutic avenue for managing glaucoma progression.
- Targeting hypoxia-related epigenetic pathways could offer novel treatment strategies for glaucoma.
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