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Advanced glycation end products cause increased CCN family and extracellular matrix gene expression in the diabetic rodent retina

机译:晚期糖基化终产物导致糖尿病啮齿动物视网膜中CCN家族和细胞外基质基因表达增加

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摘要

Aims/hypothesisReferred to as CCN, the family of growth factors consisting of cystein-rich protein 61 (CYR61, also known as CCN1), connective tissue growth factor (CTGF, also known as CCN2), nephroblastoma overexpressed gene (NOV, also known as CCN3) and WNT1-inducible signalling pathway proteins 1, 2 and 3 (WISP1, −2 and −3; also known as CCN4, −5 and −6) affects cellular growth, differentiation, adhesion and locomotion in wound repair, fibrotic disorders, inflammation and angiogenesis. AGEs formed in the diabetic milieu affect the same processes, leading to diabetic complications including diabetic retinopathy. We hypothesised that pathological effects of AGEs in the diabetic retina are a consequence of AGE-induced alterations in CCN family expression.
机译:目的/假设被称为CCN,其生长因子家族由富含半胱氨酸的蛋白61(CYR61,也称为CCN1),结缔组织生长因子(CTGF,也称为CCN2),肾母细胞瘤过表达基因(NOV,也称为CCN)组成CCN3)和WNT1诱导的信号通路蛋白1、2和3(WISP1,-2和-3;也称为CCN4,-5和-6)影响伤口修复,纤维化疾病中的细胞生长,分化,粘附和运动,炎症和血管生成。在糖尿病环境中形成的AGEs影响相同的过程,导致糖尿病并发症,包括糖尿病性视网膜病。我们假设糖尿病视网膜中AGEs的病理影响是AGE诱导CCN家族表达改变的结果。

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