griseofulvin and Retinal-Neovascularization

Ferrochelatase (FECH) is the terminal enzyme in heme biosynthesis. We previously showed that FECH is required for endothelial cell growth in vitro and choroidal neovascularization in vivo. But FECH has not been explored in retinal neovascularization, which underlies diseases like proliferative diabetic retinopathy and retinopathy of prematurity. Here, we investigated the inhibition of FECH using genetic and chemical approaches in the oxygen-induced retinopathy (OIR) mouse model. In OIR mice, FECH expression is upregulated and co-localized with neovascular tufts. Partial loss-of-function Fech

Topics: Animals; Cell Hypoxia; Cell Proliferation; Female; Ferrochelatase; Griseofulvin; Mice; Mice, Inbred C57BL; Retina; Retinal Neovascularization