Multiple Targets of A Single Molecule: A New Strategy For Glaucoma Treatment

Yanying Miao

Fudan University, Shanghai, China

Biography :

Yanying Miao received her Ph.D. degree from Peking University in 2007. She visited the University of Chicago as a scholar from 2012 to 2013. She serves as a director member of Shanghai Physiological Society. She has pub­lished more than 40 papers in reputed journals.

Abstract :

Glaucoma is an important cause of irreversible blindness, which is characterized by the loss of retinal ganglion cells and their axons. The current treatment methods cannot cure glau­coma and can only delay the course of the disease. Therefore, there is an urgent need to understand the pathogenesis of glaucoma and search for potential therapeutic targets. Rho small G protein Rac1 is an important intracellular signal transduction molecule that functions in a cell-type specific manner during physiological and pathological processes. Our work has revealed that Rac1 knockout in RGC can inhibit RGC apoptosis and alleviate axonal dysfunc­tion in an experimental glaucoma model; Rac1 knockout in astrocytes increases the survival of RGCs; Inhibition of Rac1 activity promotes ATP release from astrocytes through connexin 43 and protects RGCs from injury by adenosine receptor 3 in glaucoma. Moreover, the specific inhibition of Rac1 in microglial cells also contributes to block the damage of glaucomatous RGCs. The combined inhibition of Rac1 in glial cells and RGCs showed a more effective neu­roprotection in glaucoma. Our work suggests that Rac1, as signal hub molecule with multiple targets, may be a new potential neuroprotective candidate molecule for glaucoma treatment.