The conventional outflow pathway is the primary regulator of outflow resistance in glaucoma. This pathway consists of a series of cells and tissues that work to maintain normal intraocular pressure including the trabecular meshwork (TM), Schlemm’s canal and distal vessels. Dysfunction of the TM tissue is a major cause of elevated intraocular pressure (IOP) in glaucoma. Distal vessels play a role in regulating outflow facility and thus IOP.

 

Our lab studies these two areas of the outflow pathway to determine their specific role in IOP regulation and to assess if therapeutic interventions can be targeted to lower IOP in glaucoma. We have shown that nanoparticles known as extracellular vesicles (EVs) have significantly different cargo when released from glaucoma TM cells, and that these differences included changes in ECM protein cargo. We are currently investigating if EVs can be used as disease biomarkers to more easily detect glaucomatous disease, as well as determining if they can be used as targeted therapies to stop or reverse disease progression. Our previous studies into distal vessels have shown that they are vasoactive and can be pharmacologically regulated. We are interested in the physiology and biomechanics of distal vessels and investigating their role in IOP homeostasis in both normal and glaucoma conditions.