Critical Overview: Ocular Angiogenesis

Angiogenesis is the formation of new blood vessels from preexisting vasculature, being mediated and
regulated by a complex composed of growth factors, cytokines, cell signaling molecules and
extracellular matrix components. The most important pro-angiogenesis regulator molecules are
vascular endothelial factor (VEGF), fibroblasts growth factors (FGFs), hypoxia-inducible factor 1 (HIF-
1), platelet-derived growth factor (PDGF) and angiopoietins (Ang). Ocular angiogenesis can occur in
retina, choroid, and cornea of the eye, leading to severe visual impairment, being related to a broad
spectrum of disorders such as wet age-related macular degeneration (AMD), diabetic retinopathy
(DR), retinopathy of prematurity (ROP), neovascular glaucoma (NVG) and corneal neovascularization
(CNV). Monotherapy or laser-adjunctive inhibition of VEGF, as the humanized monoclonal anti-VEGF
antibody (Bevacizumab, Ranibizumab) and the “VEGF-trap” molecules (Aflibercept) have become the
gold standard therapy for these ocular angiogenic diseases. The current frontier of anti-angiogenic
ocular treatment lies in reducing the treatment burden of frequent injections needed and increase the
efficacy and the visual outcomes. New drugs are being developed with the goal of extending
treatment intervals and increased efficiency such as: Brolucizumab, Faricimab, Abicipar pegol and
Combercept. As a different approach to extend treatment burden, there is the Port Delivery System
that may address the irregular dosing of current treatment and launch us into an era of continuous
angiogenic suppression. This chapter Ocular Angiogenesis provide an emerging view of the clinical
features of pathological angiogenesis in the eye, the molecular mechanisms including growth factors
and other molecules involved in the pathological vessel growth, and the progress made in the
development of new treatments.