Understanding Trabecular Meshwork Physiology and its Vital Role In Glaucoma Treatment

This presentation explores the trabecular meshwork (TM) as a critical tissue in glaucoma pathology, examining cell death mechanisms accounting for TM cell death revealing that in severe glaucoma, autophagy mechanisms are upregulated, suggesting a switch from apoptosis to autophagy as TM damage progresses this could have potential diagnostic and therapeutic implications in glaucoma. The presentation also discusses very briefly the work on pseudoexfoliation glaucoma by examining miRNA, proteome signatures, and cytokine profiles in aqueous humor, tears, and TM tissues that have shed light into the TGF paradox in this entity. Our journey has led us to develop a new technique of Minimally invasive glaucoma surgery, namely microincisional trabeculectomy, which ash enabled us to revisit the anatomical variation in the TM using histopathology, Immunohistochemistry, and electron microscopy. Multi-omics analysis in the other ongoing studies may provide insights into TM cell signatures that could lead to more precise, molecular changes determining TM cell fate and differences in different glaucoma types.

Glaucoma remains a leading cause of irreversible blindness worldwide, with limited advancements in topical treatments over recent years. This presentation explores innovative therapeutic strategies targeting trabecular meshwork (TM) dysfunction, which plays a critical role in maintaining intraocular pressure (IOP) and is a key contributor to glaucoma. Dysregulation of the Rho-kinase (ROCK) signaling pathway has been linked to TM dysfunction and elevated IOP. The development of ROCK inhibitors represents a promising new class of drugs with the potential to provide effective treatments for glaucoma, as demonstrated in clinical studies.