Gulab Zode, PhD

My laboratory is interested in understanding the pathological mechanisms involved in glaucomatous damage to trabecular meshwork (TM), elevating IOP. Our primary focus is to understand the role of protein misfolding and its associated cellular processes including, endoplasmic reticulum (ER) stress and autophagy, in glaucomatous TM damage. We have developed two novel glaucoma mouse models, as well as established various genetic tools, to study protein misfolding and biological functions of unfolded protein response pathway and autophagy in glaucoma pathogenesis. Our lab has previously established the pathological role of ER stress in glaucomatous TM damage and IOP elevation. We are currently targeting these pathways using genetic and pharmacological manipulations for the treatment of glaucoma.