【摘 要】
：
系膜区基质积聚是糖尿病肾病的病理特征之一,它主要由于基质合成与降解通路的精细平衡失调。近年来研究发现高糖能通过对系膜细胞基质金属蛋白酶类(MMPs)基因转录、活化及抑
【机 构】
：
复旦大学附属中山医院内分泌科 上海200032
论文部分内容阅读
系膜区基质积聚是糖尿病肾病的病理特征之一,它主要由于基质合成与降解通路的精细平衡失调。近年来研究发现高糖能通过对系膜细胞基质金属蛋白酶类(MMPs)基因转录、活化及抑制等三方面复杂的调控而降低其基质降解活性,调控过程可能由转化生长因子(TGF)-β、胰岛素样生长因子(IGF)-1和基质糖化等介导。系膜细胞MMPs活性下降致系膜区基质降解减少可能是引起系膜区基质积聚导致糖尿病肾病的重要原因之一。
Mesangial matrix accumulation is one of the pathological features of diabetic nephropathy, which is mainly due to the delicate balance of matrix synthesis and degradation pathways. In recent years, it has been found that high glucose can reduce its matrix degradation activity through complex regulation of transcription, activation and inhibition of MMPs gene in mesangial cells. The regulation of high glucose may be mediated by transforming growth factor (TGF) -β , Insulin-like growth factor (IGF-1) and matrix glycation. Decreased mesangial matrix degradation caused by decreased MMPs activity of mesangial cells may be one of the important causes of diabetic nephropathy caused by matrix accumulation in mesangial area.
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