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Review Article

与年龄相关的黄斑变性：锌金属蛋白酶参与的现代知识

卷 20, 期 9, 2019

页: [903 - 918] 页: 16

弟呕挨: 10.2174/1389450120666190122114857

价格: $65

摘要

背景：高龄老年性黄斑变性（AMD）是导致治疗选择有限的老年人失明的主要原因。该疾病的特征在于黄斑中的光感受器丧失和视网膜色素上皮（RPE）功能降低，与基质降解，细胞增殖，新血管形成和炎症相关。基质金属蛋白酶（MMPs），解整合素和金属蛋白酶（ADAMs）以及具有血小板反应蛋白基序（ADAMTSs）的解整合素和金属蛋白酶在细胞外基质（ECM）转换的生理学中起关键作用，并且反过来在ECM病理学如AMD中起关键作用。 。 MMPs和金属蛋白酶组织抑制剂（TIMPs）的活性之间的平衡对ECM组分的完整性至关重要;实际上，这些因素的比例失调会在ECM中产生深刻的变化，包括增厚和沉积形成，最终可能导致AMD的发展。 目的：本文综述了锌金属蛋白酶对AMD发展的相关性和影响及其作为生物标志物和/或治疗靶点的作用。我们举例说明了目前用于解剖MMPs生理特性的几种MMP抑制剂的研究。此外，分析了用于控制AMD中MMP和ADAM活性的所有分子或技术。 结论：该研究强调了RPE细胞表达的MMPs活性的变化，突出了已经使用的MMP抑制剂的功能，因此表明它们作为治疗AMD的治疗剂的应用。

关键词: AMD，RPE，MMPs，ADAMs，ADAMTSs，MMP抑制剂。

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图形摘要

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