Oxygen-induced retinopathy: a model for vascular pathology in the retina

Oxygen-induced retinopathy: a model for vascular pathology in the retina
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DOI:
10.1038/eye.2009.306
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发表时间:
2010-03-01
期刊:
EYE
影响因子:
3.9
通讯作者:
Fruttiger, M.
Fruttiger, M.
中科院分区:
医学3区
文献类型:
--
作者:
Scott, A.;Fruttiger, M.

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视网膜缺血性血管疾病可能使视网膜永久性缺血,视力缓慢下降,或者导致增殖性血管疾病,这也会损害视力。为了研究导致这种病理的分子和细胞机制,人们对一种小鼠模型进行了广泛研究。该模型是基于在小鼠幼崽视网膜血管仍在发育阶段使其暴露于高氧环境。这会导致毛细血管耗竭,当回到正常空气环境时,会导致视网膜缺血以及视网膜血管的增殖性血管疾病(氧诱导视网膜病变(OIR))。许多使用这种OIR模型的研究表明,血管生成因子的调节以及炎症细胞的影响在血管发病机制中起着关键作用。在OIR模型中还证明,增殖性血管疾病并非视网膜缺血诱导血管生成的唯一可能结果,视网膜缺血区域可以由健康血管重新形成血管。因此,了解在OIR模型中控制病理性和健康血管生成之间平衡的因素可能对人类视网膜缺血性疾病具有重要意义。《眼睛》(2010年)24卷,416 - 421页;doi:10.1038/eye.2009.306;2009年12月11日在线发表
Ischaemic vascular disease in the retina may either leave retina permanently ischaemic with slow degradation of vision, or alternatively lead to proliferative vascular disease, which can also destroy vision. To investigate the molecular and cellular mechanisms that contribute to this pathology a mouse model has been studied extensively. The model is based on the exposure of mouse pups to hyperoxia during a phase when their retinal vasculature is still developing. This leads to capillary depletion, and upon return to room air, results in retinal ischaemia and proliferative vascular disease in the retinal vasculature (oxygen-induced retinopathy (OIR)). Numerous studies using this OIR model have revealed that the regulation of angiogenic factors and the influence of inflammatory cells play a pivotal role in the vascular pathogenesis. It has also been demonstrated in the OIR model that proliferative vascular disease is not the only possible outcome of ischaemia-induced angiogenesis in the retina, but that ischaemic areas in the retina can be revascularised with healthy blood vessels. Therefore, understanding the factors that control the balance between pathological and healthy angiogenesis in the OIR model may have important implications for human retinal ischaemic disease. Eye (2010) 24, 416-421; doi:10.1038/eye.2009.306; published online 11 December 2009