The pathogenesis of choroidal neovascularization in patients with age-related macular degeneration.
The pathogenesis of choroidal neovascularization in patients with age-related macular degeneration.
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发表时间：
1999-11
期刊：
影响因子：
2.2
通讯作者：
P. Campochiaro;Paul D. Soloway;Stephen J. Ryan;Joan W. Miller
中科院分区：
文献类型：
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作者：
P. Campochiaro;Paul D. Soloway;Stephen J. Ryan;Joan W. Miller
激光光凝和几种实验性治疗脉络膜新生血管（CNV）的患者年龄相关性黄斑变性试图消融新生血管，但不解决潜在的血管生成刺激。因此，递归是一个主要问题。对抗CNV生长的药物治疗将是一项重大进展，但由于缺乏对CNV发病机制中涉及的刺激和其他分子信号的了解，其发展受到阻碍。在这里，我们探索线索，可以从临床，流行病学，病理和实验数据收集。这表明视网膜色素上皮细胞（RPE）细胞外基质的异常可能促进促血管生成的RPE表型，从而促进CNV的发展。这提供了一个可以测试的一般假设，但也有必要测试有关导致CNV的基因表达特异性改变的假设。基因表达变化的识别将为合理设计药物治疗提供靶点。
Laser photocoagulation and several experimental treatments for choroidal neovascularization (CNV) in patients with age-related macular degeneration attempt to ablate the neovascularization, but do not address underlying angiogenic stimuli. As a result, recurrences are a major problem. Drug treatment to counter the growth of CNV would be a major advance, but its development is impeded by lack of knowledge concerning the stimuli and other molecular signals involved in the pathogenesis of CNV. Herein we explore clues that can be gleaned from clinical, epidemiological, pathological, and experimental data. These suggest that abnormalities of the extracellular matrix of retinal pigmented epithelial (RPE) cells may promote a pro-angiogenic RPE phenotype that contributes to the development of CNV. This provides a general hypothesis that can be tested, but it is also necessary to test hypotheses regarding the specific alterations in gene expression that contribute to CNV. Identification of alterations in gene expression will provide targets for rational design of drug treatment.