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Related Concept Videos

The Ras Gene02:38

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Related Experiment Video

Updated: Feb 9, 2026

Trabecular Meshwork Response to Pressure Elevation in the Living Human Eye
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Trabecular meshwork ECM remodeling in glaucoma: could RAS be a target?

Puneet Agarwal1, Renu Agarwal2

  • 1a Department of Ophthalmology , International Medical University, IMU Clinical School , Seremban , Malaysia.

Expert Opinion on Therapeutic Targets
|June 9, 2018
PubMed
Summary

Renin-angiotensin system (RAS) inhibitors may lower intraocular pressure (IOP) by restoring extracellular matrix (ECM) homeostasis in the eye's drainage system. This approach targets glaucoma progression by improving aqueous humor outflow.

Keywords:
Extracellular matrixintraocular pressurerenin-angiotensin systemtrabecular meshworktransforming growth factor

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Area of Science:

  • Ocular Physiology
  • Glaucoma Pathophysiology
  • Extracellular Matrix Biology

Background:

  • Extracellular matrix (ECM) homeostasis disturbances in the trabecular meshwork (TM) increase aqueous outflow resistance, elevating intraocular pressure (IOP) in glaucoma.
  • The renin-angiotensin system (RAS) is implicated in cardiovascular pathologies involving pressure overload and positively affects ECM homeostasis.
  • RAS components are present in ocular tissues and play a role in regulating aqueous humor dynamics.

Purpose of the Study:

  • To summarize current evidence on RAS components in ocular tissue and their role in aqueous humor dynamics.
  • To discuss the role of RAS in ECM remodeling, including synthesis and breakdown.
  • To explore the mechanisms of ECM remodeling involving RAS interactions with key signaling pathways in ocular tissue.

Main Methods:

  • Literature review of existing evidence on RAS in ocular tissues.
  • Discussion of RAS involvement in ECM synthesis and degradation.
  • Analysis of molecular interactions between RAS and signaling pathways (TGF-β, Wnt/β-catenin, BMPs, CTGF, MMPs) in the TM.

Main Results:

  • RAS plays a significant role in ECM remodeling within the TM of hypertensive eyes.
  • RAS inhibition demonstrates a potential to restore ECM homeostasis in ocular outflow pathways.
  • The IOP-lowering effects of RAS inhibitors are likely linked to improved ECM homeostasis rather than solely vascular effects.

Conclusions:

  • Restoring ECM homeostasis in the TM is a rational strategy for managing glaucoma progression.
  • RAS inhibitors show promise in treating glaucoma by targeting ECM remodeling in the TM.
  • Further research is needed to explore the broader mechanistic targets and consequences of RAS inhibitors in the TM.