Research in our laboratory focuses on mechanistic and therapeutic studies of retinal degenerative diseases caused by loss of photoreceptors or retinal ganglion cells, such as age-related macular degeneration, retinitis pigmentosa, and glaucoma. These degenerative conditions affect millions of people in the US leading to vision impairment and blindness. To restore visual function, my laboratory is pursuing two strategies: neuroprotection (to slow down or prevent the death of retinal neurons) and neuroregeneration (to generate new retinal neurons). Our research targets the following 4 main areas: (1) For neuroprotection of retinal ganglion cells, the sole output neurons in the retina, we investigate various signaling pathways when ganglion cells and their axons are damaged by diverse injuries from optic nerve crush, excitotoxicity, and elevated intraocular pressure, and whether targeted manipulation of these pathways saves ganglion cells and restores visual function. (2) For neuroregeneration, we examine the regenerative capability of Müller glia (MG), the primary glial cell type in the mammalian retina. The goal is to reprogram MG in vivo to generate MG-derived retinal stem cells that are capable of differentiating to new retinal neurons for vision restoration. (3) We study axon regeneration after CNS injury. Unlike neurons in the peripheral nervous system, CNS axons fail to regenerate after injury. Using optic nerve crush in mice to model adult CNS injury, we investigate the intrinsic cell growth pathways that can be manipulated in order to activate the re-growth of axons from retinal ganglion cells. (4) For neuroprotection of photoreceptors, we investigate the molecular mechanisms underlying photoreceptor degeneration using animal models of retinal degenerative diseases. Our studies focus on signal transduction pathways that promote photoreceptor survival in the presence of genetic and environmental insults.