系膜细胞能合成基膜和系膜基质(mesangial matrix)的成分，还可吞噬和降解沉积在基膜上的免疫复合物，以维持基膜的通透性。并参与基膜的更新和修复。
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The main expression of DN is glomerulosclerosis and tubulointerstitial fibrosis. TGF-β1 systems is activated by high glucose in DM,and Smad2 proteins can increase the secretion of extracellular matrix(ECM)through transfer TGF-βsignaling,which can make glomerular basement membrane thicker and result in DN.
DN主要表现为肾小球硬化和肾小管间质纤维化,DM的高糖状态下TGF-β1系统激活,Smad2蛋白可通过转导TGF-β信号促进细胞外基质(extracellularmatrix,ECM)的合成与沉积,使系膜基质增多,肾小球毛细血管基底膜增厚,致糖尿病肾病的发生发展。
参考来源 - Smad2反义寡核苷酸对高糖培养人肾小球系膜细胞分泌纤连蛋白，层粘连蛋白的影响·2,447,543篇论文数据，部分数据来源于NoteExpress
目的：探讨肾疏宁防治系膜基质硬化的细胞分子机制。
Objective: To study the cellular and molecular mechanism of Shenshuning (SSN) in preventing mesangial sclerosis.
系膜细胞核不规则，胞质内线粒体肿胀，系膜基质正常。
Mesangial cell nuclei showed irregular shape and mitochondria swelled, stroma was normal.
有关糖尿病肾病发病机制的研究，人们早先关注的是肾脏系膜基质堆积和肾小球基底膜增厚。
Research on the mechanism of diabetic nephropathy was initially focused on the mesangial matrix and glomerular basement membrane.
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