Glaucoma is the leading cause of irreversible blindness worldwide and is characterized by a specific pattern of retinal ganglion cell (RGC) loss; however, pathogenic mechanisms of this disease are not fully understood. At present, the sole modifiable risk factor for glaucomatous RGC loss is intraocular pressure (IOP), and current therapeutic strategies aim to lower IOP.

The role of lamina cribrosa biomechanics in glaucoma

Studies have shown that the site of RGC injury in glaucoma occurs at the lamina cribrosa (LC), a porous collagenous network housing LC cells and astrocytes, that provides structural support to RGC axons as they exit the globe. A prevailing theory suggests that the inciting injury in glaucoma is biomechanical strain on the LC induced by IOP elevation, causing direct mechanical failure of the LC collagen matrix.

A primary research interest of our laboratory is the investigation of LC biomechanics in response to dynamic IOP fluctuation. We are examining LC biomechanics on the microscopic and ultrastructural level using human cadaver eyes, and utilizing a LC organoid system to investigate cellular mechanisms that alter LC biomechanical response to IOP. Together, we hope to elucidate mechanisms by which RGC axon function is altered.

The role of the chemokine CXCL12 in trabecular meshwork cell homeostasis

The mechanism of IOP increase in glaucoma is primarily due to dysfunction and aging of the trabecular meshwork, the outflow tract for aqueous humor in the eye. In collaboration with Dr. Samuel Herberg, we are investigating the role of a vital chemokine, CXCL12/SDF-1, in trabecular meshwork pathophysiology and its function as a chemoattractant for mesenchymal stem cell therapy of high-pressure glaucoma.