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Pathogenesis of glaucoma: Extracellular matrix dysfunction in the trabecular meshwork-A review
Kate E Keller1, Donna M Peters2
1Casey Eye Institute, Oregon Health &Science University, Portland, Oregon, USA.
Clinical & Experimental Ophthalmology
|January 17, 2022
Summary
Changes in the eye's trabecular meshwork extracellular matrix (ECM) can increase outflow resistance and intraocular pressure (IOP), a key factor in glaucoma development.
Area of Science:
- Ophthalmology
- Cell Biology
- Biochemistry
Background:
- The trabecular meshwork (TM) controls aqueous humor outflow, regulating intraocular pressure (IOP).
- TM outflow resistance is determined by cellular and extracellular matrix (ECM) interactions.
- Dysregulation of TM homeostasis elevates IOP, a major risk factor for glaucoma.
Purpose of the Study:
- To review alterations in the TM's ECM structure and function.
- To examine the impact of ECM changes on TM cell behavior.
- To discuss the relationship between ECM modifications, outflow resistance, and glaucoma pathogenesis.
Main Methods:
- Literature review focusing on ECM remodeling in the trabecular meshwork.
- Analysis of molecular interactions within the ECM.
- Discussion of cellular responses to ECM changes.
Main Results:
- ECM remodeling influences TM structure and function.
- Altered ECM composition and molecular interactions increase outflow resistance.
- Subtle and gross ECM changes impact TM cell behavior and IOP.
Conclusions:
- Trabecular meshwork ECM modifications are critical in regulating aqueous humor outflow.
- Changes in ECM homeostasis contribute to elevated IOP and glaucoma.
- Understanding ECM dynamics in the TM is essential for glaucoma research.
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