Research Paper Volume 15, Issue 1 pp 37—52
Genetic deficiency and pharmacological modulation of RORα regulate laser-induced choroidal neovascularization
Figure 7. A schematic model for the effects of RORα on regulating CNV in wet AMD. Deficiency of RORα in choroid vessels directly induces expression of VEGF receptor VEGFR2, leading to enhanced choroidal endothelial angiogenic response and exacerbated pathological CNV formation. RORα deficiency may also influence CNV via increased TNFα, and chronic inflammation in the choroidal local environment, to potentially sensitize VEGF angiogenic response and thereby CNV formation. Abbreviations: BrM: Bruch’s membrane; CNV: choroidal neovascularization; Mc: microglial cell; Mp: macrophage; RPE: retinal pigment epithelium.