I study the molecular mechanisms determining intraocular pressure (IOP) elevation, which is a major risk factor for glaucoma. IOP results from a resistance to drainage of aqueous humor (AqH) through outflow structures that reside in the angle between the cornea and the iris. AqH outflow structures, which include the trabecular meshwork (TM) and Schlemm’s canal (SC), are critical to maintaining IOP homeostasis. An increase in resistance to AqH outflow resulting from dysfunction of the TM and SC cells causes elevated IOP and glaucoma. Using mouse models, I am investigating the genes and pathways of the AqH outflow structures involved in IOP regulation. Glaucoma therapy is based on reducing IOP but more effective treatments are needed. Greater knowledge of outflow structure biology is required for the rational development of new treatments. Thus the ultimate goal of my work is to uncover molecular targets to lower IOP in glaucoma patients.
BA, Behavioral Neuroscience, Connecticut College, New London, CT