Summary

Currently, the first-line treatment for wet AMD is to block the function of vascular endothelial growth factor (VEGF), a major factor promoting the growth of new blood vessels in the eye. Besides the high costs, these treatments are injected into the eyeball using syringes, which is complicated and can be dangerous. Based on a novel finding from our lab, that ascorbate (vitamin C) plays a role in regulating the function of the genome, this research aims to use vitamin C to inhibit the production of VEGF in the eye, thus blocking its function. Successful completion of this research will help develop an ascorbate treatment to delay and/or prevent disease progression that is inexpensive and readily available for AMD patients.

Project Details

This research aims to develop a prevention of AMD by vitamin C (ascorbate), which may inhibit intraocular VEGF signaling. We will first examine the effect of ascorbate on VEGF expression in human retinal pigmented epithelium (RPE) cells. The mechanism by which ascorbate inhibits VEGF will be examined by high-throughput sequencing technology. After that, ascorbate will be tested in modeled mice to see if VEGF overexpression and choroidal neovascularization can be prevented by the treatment. Currently, the first-line treatment for wet AMD is to block the function of VEGF, a major factor promoting the growth of new blood vessels in the eye. These treatments are costly and complicated to perform, requiring injections into the eyeball. Furthermore, anti-VEGF therapies only temporarily block the action of VEGF, but have no effect on the continued production of VEGF within the eye. Based on a novel finding from our lab, of ascorbate’s ability to regulate the function of the genome, this research aims to use vitamin C to inhibit the production of VEGF in the eye, thus blocking its function. Successful completion of this project will help to develop an ascorbate treatment to delay and/or prevent AMD progression that is inexpensive and readily available for AMD patients