Guo-Hua Fong

Angiogenesis, the growth of new microvessels, is a double-edged sword: it is essential for normal tissue growth and repair but is also associated with a variety of diseases such as tumorigenesis, neovascular age-related macular degeneration (nAMD), retinopathy of prematurity (ROP), and proliferative diabetic retinopathy (PDR). Pathological angiogenesis (aka neovascularization) typically goes on excessively and produces leaky microvessels. In ocular diseases such as nAMD, ROP, and PDR, blood contents leak out of aberrantly formed microvessels, leading to edema, tissue damage, and blindness at advanced stages. We are studying neovascularization in animal models of nAMD and ROP and exploring therapeutic opportunities. Developing novel anti-angiogenesis strategies for nAMD. Using novel mouse models, we are improving the long-term safety of anti-VEGFA therapies and developing VEGF-independent anti-angiogenesis strategies. Exploring the feasibility of preventing ROP. We are investigating mechanisms of oxygen-induced retinal capillary obliteration, with the long-term goal of preventing ROP by protecting retinal capillaries during oxygen exposure. Repairing lost retinal vascular network. We are studying retinal vascular obliteration in the mouse model of oxygen-induced retinopathy, a proxy of ROP. These studies are expected to help repair damaged retinal vascular network, thus improving perfusion and alleviating hypoxia.

[2024] Endothelial HIF2α suppresses retinal angiogenesis in neonatal mice by upregulating NOTCH signaling. [2023] Prolonged hypoxia alleviates prolyl hydroxylation-mediated suppression of RIPK1 to promote necroptosis and inflammation. [2023] Tailless and hypoxia inducible factor-2α cooperate to sustain proangiogenic states of retinal astrocytes in neonatal mice. [2022] Dependence of Retinal Pigment Epithelium Integrity on the NRF2-Heme Oxygenase-1 Axis.