Glucose/lipid metabolism and vessel development in phase I ROP

ROP是儿童失明的主要原因，在美国每年约有16，000名早产儿受其折磨1。ROP 由于更多的体外受精导致更多的多胞胎和低出生率，发病率正在上升 重量.此外，越来越多的低胎龄婴儿存活下来。氧气补充在更高的水平， 更多ROP目前的ROP治疗（激光光凝和抗VEGF治疗）并不总是有效的， 长期抗VEGF治疗可能会损害大脑和器官发育。我们需要找到方法 早期治疗以防止I期ROP，从而防止新血管形成。高血压及相关 血脂异常，常见于早产儿，与ROP的发展有关，可能有助于 第一阶段ROP中的血管损失。我们必须了解开发安全有效治疗的机制， 早期ROP以防止晚期II期新血管形成。我们初步发现成纤维细胞生长因子21 FGF 21是一种重要的葡萄糖/脂质代谢调节剂，可防止视网膜血管延迟。 第一阶段ROP。因此，我们建议， 在血脂异常/高血糖加重的I期ROP中，FGF 21改善了血糖/血脂 代谢和血管发育。 在具有新生儿代谢功能障碍的ROP的小鼠模型（NMD-ROP）中，我们将检查1）FGF 21是否 改善视网膜血管发育; 2）FGF 21对脂质/葡萄糖代谢的影响; 3）FGF 21促进视网膜血管发育; 4）FGF 21促进视网膜血管发育; 5）FGF 21促进视网膜血管发育; 6）FGF 21促进视网膜血管发育; 7）FGF 21促进视网膜血管发育; 8）FGF 21促进视网膜血管发育; 9）FGF 21促进视网膜血管发育。 通过调节神经胶质细胞代谢和血管生成因子来促进正常血管形成。 本研究将确定1）FGF 21在一种新的高血糖加重I期小鼠模型中的作用 ROP; 2）FGF 21对视网膜脂质和葡萄糖利用的代谢影响; 3）视网膜神经胶质细胞的作用。 支持视网膜血管生长的代谢。FGF 21可能在早期预防和治疗ROP。

ROP, a leading cause of blindness in children, afflicts ~16,000 premature infants yearly in the US1. ROP incidence is increasing because of more in vitro fertilization resulting in more multiple births with lower birth weight. Also, increasingly low gestational age infants survive. Oxygen is supplemented at higher levels with more ROP. Current ROP treatments (laser photocoagulation and anti-VEGF therapy) are not always effective, and long-term anti-VEGF therapy may potentially impair brain and organ development. We need to find ways to treat early to prevent phase I ROP, and thus prevent neovascularization. Hyperglycemia and associated dyslipidemia, commonly see in preterm infants and associated with ROP development, may contribute to vessel loss in phase I ROP. We must understand the mechanism to develop safe and effective treatment for early ROP to prevent late phase II neovascularization. We preliminarily found that fibroblast growth factor 21 (FGF21), a significant glucose/lipid metabolic modulator, prevents retinal vascular delay in a mouse model of phase I ROP. Therefore, we propose that In dyslipidemia/hyperglycemia-exacerbated phase I ROP, FGF21 improves glucose/lipid metabolism and vessel development. In the mouse model of ROP with neonatal metabolic dysfunction (NMD-ROP), we will examine if 1) FGF21 improves retinal vascular development; 2) FGF21 effect on lipid/glucose metabolism; 3) does FGF21 promote normal vascularization by regulating glial cell metabolism and angiogenic factors. This study will determine 1) the role of FGF21 in a novel mouse model of hyperglycemia-exacerbated phase I ROP; 2) the metabolic impact of FGF21 on retinal lipid and glucose use; 3) the role of retinal glial cell metabolism in supporting retinal vessel growth. FGF21 may prevent and treat ROP at an early stage.