title: Understanding retinopathy of prematurity: update on pathogenesis.
abstract: Retinopathy of prematurity (ROP), an ocular disease characterized by the onset of vascular abnormalities in the developing retina, is the major cause of visual impairment and blindness in premature neonates. ROP is a complex condition in which various factors participate at different stages of the disease leading to microvascular degeneration followed by neovascularization, which in turn predisposes to retinal detachment. Current ablative therapies (cryotherapy and laser photocoagulation) used in the clinic for the treatment of ROP have limitations and patients can still have long-term effects even after successful treatment. New treatment modalities are still emerging. The most promising are the therapies directed against VEGF; more recently the use of preventive dietary supplementation with ω-3 polyunsaturated fatty acid may also be promising. Other than pharmacologic and nutritional approaches, cell-based strategies for vascular repair are likely to arise from advances in regenerative medicine using stem cells. In addition to all of these, a greater understanding of other factors involved in regulating pathologic retinal angiogenesis continues to emerge, suggesting potential targets for therapeutic approaches. This review summarizes an update on the current state of knowledge on ROP from our and other laboratories, with particular focus on the role of nitro-oxidative stress and notably trans-arachidonic acids in microvascular degeneration, semaphorin 3 operating as vasorepulsive molecules in the avascular hypoxic retina and in turn impairing revascularization, succinate and its receptor GPR91 in neuron-mediated retinal neovascularization, and ω-3 lipids as modulators of preretinal neovascularization.
authors.affiliation: Department of Pediatrics, Ophthalmology and Pharmacology, Centre Hospitalier Universitaire Sainte-Justine Research Center, Montréal, Qué., Canada.
authors.forename: José Carlos
authors.initials: JC
authors.lastname: Rivera
authors.forename: Przemyslaw
authors.initials: P
authors.lastname: Sapieha
authors.forename: Jean-Sébastien
authors.initials: JS
authors.lastname: Joyal
authors.forename: François
authors.initials: F
authors.lastname: Duhamel
authors.forename: Zhuo
authors.initials: Z
authors.lastname: Shao
authors.forename: Nicholas
authors.initials: N
authors.lastname: Sitaras
authors.forename: Emilie
authors.initials: E
authors.lastname: Picard
authors.forename: Ellen
authors.initials: E
authors.lastname: Zhou
authors.forename: Pierre
authors.initials: P
authors.lastname: Lachapelle
authors.forename: Sylvain
authors.initials: S
authors.lastname: Chemtob
mesh_terms: D005865:Gestational Age; D006801:Humans; D007231:Infant, Newborn; D007234:Infant, Premature; D015227:Lipid Peroxidation; D009389:Neovascularization, Pathologic; D018384:Oxidative Stress; D010100:Oxygen / Q000502:physiology / Q000627:therapeutic use; D043562:Receptors, G-Protein-Coupled; D012160:Retina / Q000196:embryology; D012171:Retinal Vessels / Q000196:embryology; D012178:Retinopathy of Prematurity / Q000209:etiology* / Q000517:prevention & control / Q000628:therapy; D012307:Risk Factors; D039961:Semaphorins; D019802:Succinic Acid; D042461:Vascular Endothelial Growth Factor A
chemical_list: D043562:Receptors, G-Protein-Coupled; C557078:SUCNR1 protein, human; D039961:Semaphorins; D042461:Vascular Endothelial Growth Factor A; D019802:Succinic Acid; D010100:Oxygen