作者: M.S. Razzaque , T. Naito , T. Taguchi
DOI: 10.1159/000046034
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摘要: Most forms of advanced glomerular diseases, if not all, are characterized by abnormal turnover extracellular matrix (ECM) proteins in glomeruli, resulting structural alterations basement membrane and mesangial matrix, usually leading to proteinuria. It is, therefore, important elucidate the regulatory mechanisms ECM metabolism diseases. Various types collagens, laminin, fibronectin, sulfated proteoglycans normal components [1– 5]. In vivo vitro studies have shown that these produced visceral epithelial cells [6, 7]. has also been demonstrated phenotypically altered activated renal mainly responsible for increased production as well diseasespecific expressed kidney [8–11]. Several lines evidence now suggest an imbalance between synthesis degradation is closely associated with accumulation subsequent progression diseases [12]. Matrix metalloproteinases (MMPs) tissue inhibitors (TIMPs) reported play role remodeling various [13, 14]. Recent proto-oncogene Ets-1 plays a transcriptional regulation proteinases such MMP-3 u-PA [15–19]. We summarize herein existing information about possible roles other functions