My laboratory is interested in understanding the pathological mechanisms involved in glaucomatous damage to trabecular meshwork (TM) and retinal ganglion cells (RGCs). Our primary focus is to understand the role of protein misfolding and its associated cellular processes including endoplasmic reticulum (ER) stress and autophagy in the glaucomatous TM damage.
We have developed two novel glaucoma mouse models and have established various genetic tools to study protein misfolding and biological functions of unfolded protein response pathway and autophagy in glaucoma pathogenesis. We are currently pursuing gene therapy via CRISPR genome editing and small chemicals to develop targeted treatment for primary open angle glaucoma.