Patschan D, Patschan S, Müller G A
Department of Nephrology and Rheumatology, University Medical Center, Robert-Koch-Straße 40, 37075 Göttingen, Germany.
Int J Nephrol. 2011;2011:828369. doi: 10.4061/2011/828369. Epub 2011 Apr 27.
Acute ischemic kidney injury is the most frequent cause of acute renal failure in daily clinical practice. It has become increasingly recognized that microvascular endothelial cell dysfunction (ED) in peritubular capillaries inhibits the process of postischemic renal reperfusion. ED can serve as therapeutic target in the management of acute ischemic kidney injury. Postischemic reflow can be restored by systemic administration of either mature endothelial cells or of endothelial progenitor cells. Endothelial progenitor cells EPCs can be cultured from the peripheral circulation of humans and different animals. The cells act vasoprotectively by direct and indirect mechanisms. The protective effects of EPCs in acute ischemic kidney injury can be stimulated by preincubating the cells with different agonistic mediators. This paper summarizes the currently available data on strategies to improve the renoprotective activity of EPCs in acute ischemic kidney injury.
急性缺血性肾损伤是日常临床实践中急性肾衰竭最常见的原因。人们越来越认识到,肾小管周围毛细血管中的微血管内皮细胞功能障碍(ED)会抑制缺血后肾脏再灌注过程。ED可作为急性缺血性肾损伤治疗的靶点。通过全身给予成熟内皮细胞或内皮祖细胞可恢复缺血后再灌注。内皮祖细胞(EPCs)可从人类和不同动物的外周循环中培养获得。这些细胞通过直接和间接机制发挥血管保护作用。用不同的激动剂介质预孵育细胞可增强EPCs在急性缺血性肾损伤中的保护作用。本文总结了目前关于提高EPCs在急性缺血性肾损伤中肾脏保护活性策略的可用数据。