Ocular neovascularization: basic mechanisms and therapeutic advances.
The vast majority of diseases that cause catastrophic loss of vision do so as a result of ocular neovascularization. During normal retinal vascular development, vascular endothelial cells proliferate and migrate through the extracellular matrix in response to a variety of cytokines, leading to the formation of new blood vessels in a highly ordered fashion. During abnormal neovascularization of the iris, retina, or choroid, angiogenesis is unregulated and usually results in the formation of dysfunctional blood vessels. When these newly formed vessels leak fluid, hemorrhage, or are associated with fibrous proliferation, retinal edema, retinal/vitreous hemorrhage, or traction retinal detachments may occur resulting in potentially catastrophic loss of vision. In this review, we will briefly discuss the scope of the clinical problem and the general underlying principles of angiogenesis. We will focus on recent laboratory advances that have led to the development of therapeutics useful in the treatment of neovascular eye diseases. We will describe compounds currently in pre-clinical development stages as well as the results of clinical trials involving the use of these drugs as treatments for ocular neovascularization.
Dorrell
Michael
M
Department of Cell Biology, The Scripps Research Institute, Department of Ophthalmology, Scripps Clinic, La Jolla, California 92014, USA.
Uusitalo-Jarvinen
Hannele
H
Aguilar
Edith
E
Friedlander
Martin
M
D020533:Angiogenesis Inhibitors / Q000627:therapeutic use*; D020256:Choroidal Neovascularization / Q000188:drug therapy / Q000503:physiopathology*; D002986:Clinical Trials as Topic; D006801:Humans; D007498:Iris / Q000098:blood supply*; D009389:Neovascularization, Pathologic / Q000188:drug therapy / Q000503:physiopathology*; D015861:Retinal Neovascularization / Q000188:drug therapy / Q000503:physiopathology*
D020533:Angiogenesis Inhibitors