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在肾素-血管紧张素-醛固酮系统(RAS)活化参与多器官损伤(包括糖尿病肾小球硬化)过程中,血管紧张素(AngiotensinⅡ,AngⅡ)起着重要的介导作用[1]。AngⅡ作为RAS中最具活性的成分,也是引起肾脏损伤的重要因子。AngⅡ不仅可引起肾内血流动力学改变,还可通过直接激活炎症细胞调节多种炎症介质的表达,参与肾脏损伤过程[2],引起肾小管细胞、系膜细胞增生肥大,使细胞外基质(ExtracellularMatrix,ECM)过度沉积和降解减少,诱导肾小管上皮细胞发生表型转化、凋亡等,从而加速糖尿病肾损害的进展。
AngiotensinⅡ (AngⅡ) plays an important role in the activation of the renin-angiotensin-aldosterone system (RAS) in multiple organ injury (including diabetic glomerulosclerosis) [1]. AngⅡ, the most active component of RAS, is also an important factor that causes kidney damage. Ang Ⅱ not only can cause renal hemodynamic changes, but also through the direct activation of inflammatory cells to regulate the expression of a variety of inflammatory mediators involved in the process of renal injury [2], causing tubular cells, mesangial cells hypertrophy, the extracellular matrix (ExtracellularMatrix, ECM) over-deposition and degradation of reduced, induced tubular epithelial cells phenotypic transformation, apoptosis, thereby accelerating the progression of diabetic nephropathy.