Kermorvant-Duchemin E, Sennlaub F, Behar-Cohen F, Chemtob S
Service de Réanimation Pédiatrique et Néonatale, Hôpital Necker-Enfants Malades, 149 rue de Sèvres 75015 Paris, France.
Arch Pediatr. 2011 Jul;18 Suppl 2:S79-85. doi: 10.1016/S0929-693X(11)71095-8.
Retinopathy of prematurity (ROP) is a major cause of visual impairment in premature infants. It is characterized by an arrest in normal retinal vascular development associated with microvascular degeneration, followed by an abnormal hypoxiainduced neovascularization. Recent studies point out that ROP is a multifactorial disease, implicating both oxygen-dependent and oxygen-independent mechanisms. Oxygen-dependent factors leading to microvascular degeneration include generation of reactive oxygen species and suppression of specific oxygen-regulated vascular survival factors, such as vascular endothelial growth factor (VEGF) and erythropoietin. The other major mechanism for the initial capillary loss is oxygen-independent and implicates a deficit in growth factor IGF-1/IGFBP3. The proliferative, second phase of ROP is triggered by increases in vascular growth factors concentrations, in an attempt to compensate for the hypoxic retina. Novel signaling pathways for vascular repair, implicating both metabolite signaling and inflammatory lipids signaling, represent new therapeutic avenues for ROP.
早产儿视网膜病变（ROP）是导致早产儿视力损害的主要原因。其特征是正常视网膜血管发育停滞，伴有微血管变性，随后出现异常的缺氧诱导性新生血管形成。最近的研究指出，ROP是一种多因素疾病，涉及氧依赖性和非氧依赖性机制。导致微血管变性的氧依赖性因素包括活性氧的产生以及对特定氧调节血管存活因子（如血管内皮生长因子（VEGF）和促红细胞生成素）的抑制。最初毛细血管丧失的另一个主要机制是非氧依赖性的，与生长因子IGF-1/IGFBP3缺乏有关。ROP的增殖性第二阶段是由血管生长因子浓度增加触发的，试图补偿缺氧的视网膜。涉及代谢物信号传导和炎症脂质信号传导的新型血管修复信号通路，为ROP提供了新的治疗途径。
