Carboxyethylpyrrole adducts, age-related macular degeneration and neovascularization.
Carboxyethylpyrrole adducts, age-related macular degeneration and neovascularization.
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DOI：
10.1007/978-0-387-74904-4_30
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发表时间：
2008
影响因子：
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通讯作者：
K. Renganathan;Q. Ebrahem;A. Vasanji;X. Gu;Liang Lu;J. Sears;R. G. Salomon;B. Anand-Apte;J. Crabb
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文献类型：
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作者：
K. Renganathan;Q. Ebrahem;A. Vasanji;X. Gu;Liang Lu;J. Sears;R. G. Salomon;B. Anand-Apte;J. Crabb
年龄相关性黄斑变性（AMD）晚期的脉络膜新生血管（CNV）涉及从脉络膜毛细血管通过Bruch膜和视网膜色素上皮（RPE）的异常血管生长，并且在所有AMD患者中占严重衰弱性视力丧失的80%以上。与AMD发病机制和CNV的发展相关的分子机制仍然知之甚少。我们假设氧化蛋白修饰是AMD发病机制中的主要催化剂，并且在CNV的发展中起作用（Crabb et al.，2002年）。氧化损伤长期以来一直被怀疑是导致AMD的原因（Beatty等人，2000），得到了吸烟增加AMD风险的间接证据的支持（Seddon等人，1996），抗氧化剂维生素和锌可以减缓选定个体的疾病进展（AREDS，2001）。
Choroidal neovascularization (CNV) in late stage age-related macular degeneration (AMD) involves abnormal vessel growth from the choriocapillaris through Bruch’s membrane and the retinal pigment epithelium (RPE) and accounts for more than 80%of the severe debilitating vision loss in all AMD patients. The molecular mechanisms associated with AMD pathogenesis and the development of CNV remain poorly understood.We hypothesize that oxidative protein modifications are primary catalysts in AMD pathogenesis and play a role in the development of CNV (Crabb et al., 2002). Oxidative damage has long been suspected of contributing to AMD (Beatty et al., 2000), supported by indirect evidence that smoking increases the risk of AMD (Seddon et al., 1996) and that antioxidant vitamins and zinc can slow disease progression for select individuals (AREDS, 2001).