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早产儿视网膜病变的发病机制。

Pathogenesis of retinopathy of prematurity.

作者信息

Smith L E H

机构信息

Department of Ophthalmology, Children's Hospital, Harvard Medical School, 300 Longwood Drive, Boston, MA 02115, USA.

出版信息

Acta Paediatr Suppl. 2002;91(437):26-8. doi: 10.1111/j.1651-2227.2002.tb00157.x.

DOI:10.1111/j.1651-2227.2002.tb00157.x
PMID:12200894
Abstract

UNLABELLED

Retinopathy of prematurity (ROP) is a blinding disease, initiated by delayed retinal vascular growth after premature birth. There are both oxygen-regulated and non-oxygen-regulated factors, which contribute to both normal vascular development and retinal neovascularization. One important oxygen-regulated factor, critical to both phases of ROP, is vascular endothelial growth factor (VEGF). A critical non oxygen-regulated growth factor is insulin-like growth factor (IGF-1). In knockout mice, lack of IGF-1 prevents normal retinal vascular growth, despite the presence of VEGF, important to vessel development. In vitro, low IGF-1 prevents vascular endothelial growth factor-induced activation of Akt, a kinase critical for vascular endothelial cell survival. Premature infants who develop ROP have lower levels of serum IGF-1 than age-matched infants without disease.

CONCLUSION

IGF-1 is critical to normal vascular development. Low IGF-1 predicts ROP and restoration of IGF-1 to normal levels may prevent ROP.

摘要

未标注

早产儿视网膜病变(ROP)是一种致盲性疾病,由早产后视网膜血管生长延迟引发。存在氧调节和非氧调节因子,它们对正常血管发育和视网膜新生血管形成均有作用。血管内皮生长因子(VEGF)是一种对ROP两个阶段都至关重要的重要氧调节因子。一种关键的非氧调节生长因子是胰岛素样生长因子(IGF-1)。在基因敲除小鼠中,尽管存在对血管发育重要的VEGF,但缺乏IGF-1会阻止正常视网膜血管生长。在体外,低水平的IGF-1会阻止血管内皮生长因子诱导的Akt激活,Akt是一种对血管内皮细胞存活至关重要的激酶。发生ROP的早产儿血清IGF-1水平低于无该疾病的年龄匹配婴儿。

结论

IGF-1对正常血管发育至关重要。低水平的IGF-1预示着ROP,将IGF-1恢复到正常水平可能预防ROP。

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