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Review Article

年龄相关性黄斑变性的发病机制中补体系统蛋白和基质金属蛋白酶的分子机制

卷 19, 期 10, 2019

页: [705 - 718] 页: 14

弟呕挨: 10.2174/1566524019666190828150625

价格: $65

摘要

年龄相关性黄斑变性（AMD）是一种眼病，主要影响50岁以上的老年人，其中视网膜的黄斑区域退化，导致中央视力丧失。与AMD发病机理相关的关键因素是年龄，吸烟，饮食和遗传风险因素。很少有相关且合理的基因参与AMD发病机制。补体基因附近的常见遗传变异（在人群中次要等位基因频率> 5％）解释了AMD遗传力的40-60％。补体系统是一组蛋白质，它们共同作用以破坏外来入侵者，引发炎症并清除细胞和组织中的碎片。包括CFH在内的几种补体系统基因及其周围的遗传变化有助于玻璃疣的形成和AMD的进展。同样，通常参与组织重塑的基质金属蛋白酶（MMP）在AMD的发病机理中也起着关键作用。 MMP参与视网膜下方细胞碎片和脂质沉积物的降解，但是随着年龄的增长，它们的功能受到影响并导致玻璃膜疣形成，继而导致黄斑变性。在这篇综述中，综述了AMD病理学，有关补体系统蛋白和MMP在眼中的正常和病理作用的现有知识。已经收集并详细讨论了补体系统蛋白，MMP，小肠异生和脂融合的分散数据。这可能会为理解AMD病理生理学的分子机制增加新的维度，并可能有助于寻找AMD的新治疗选择。

关键词: 较高年龄的疾病，玻璃膜疣形成，基于遗传的发病机制，AMD治疗方法，AMD中的补体参与，基质金属蛋白酶。

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