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The trabecular meshwork (TM) is a vital organ in glaucoma, acting as more than a passive filter. Its cells actively respond to stress, and TM dysfunction elevates intraocular pressure (IOP), leading to vision loss.

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Area of Science:

  • Ocular Physiology
  • Glaucoma Pathophysiology
  • Cell Biology

Background:

  • The trabecular meshwork (TM) regulates aqueous humor outflow from the anterior chamber to Schlemm's canal (SC).
  • Previously considered a passive filter, the TM is now recognized as a dynamic organ with active cellular functions.
  • TM dysfunction is implicated in high-tension glaucomas and subsequent vision impairment.

Purpose of the Study:

  • To elucidate the complex cellular mechanisms of the trabecular meshwork (TM).
  • To understand the TM's role in maintaining intraocular pressure (IOP) and its failure in glaucoma.
  • To explore the impact of oxidative stress on TM cell function and integrity.

Main Methods:

  • Review of current literature on TM structure and function.
  • Analysis of cellular components including cytoskeleton, extracellular matrix, and signaling pathways.
  • Investigation of the effects of aging and oxidative stress on TM physiology.

Main Results:

  • TM cells possess a cytoskeleton enabling shape changes and signaling to the nucleus.
  • TM cells actively secrete extracellular matrix, express cytokines, and perform phagocytosis/autophagy.
  • Oxidative stress impairs TM function, leading to cell decay, inflammation, and increased IOP, ultimately causing ganglion cell apoptosis.

Conclusions:

  • The trabecular meshwork (TM) is a complex, active tissue crucial for maintaining ocular health.
  • Dysfunction of the TM, particularly due to oxidative stress, is a key factor in the development of high-tension glaucoma.
  • TM failure initiates a cascade leading to retinal ganglion cell apoptosis and vision loss.