诸多原因可造成肾脏损伤,而肾小管损伤和肾间质纤维化是各种病因所致慢性肾脏病发展至终末期肾病的共同途径。炎症免疫反应是肾损伤的主要病理生理机制,并受局部微环境的精细调控。在此基础上,经历了一个损伤。修复平衡或失衡过程,从而决定着肾组织损伤与修复的走向。肾小管上皮细胞(renal tubular epithelial cell,RTEC)是兼有免疫调节作用且生物学功能十分活跃的细胞,其在肾损伤的局部微环境形成及调控中发挥重要作用。在肾损伤初始及随后的损伤修复中,RTEC不仅合成分泌各种黏附分子、趋化因子及炎症介质,招募单核/巨噬细胞、淋巴细胞等炎症细胞浸润;亦可转分化为免疫细胞或成纤维细胞,启动、参与并调控局部炎症免疫反应,行使免疫防御和损伤修复作用,在损伤因素持续存在且组织修复失衡状况下,积极参与免疫损伤以及肾间质纤维化的演变过程。因此从这个意义上说,RTEC可能是决定肾损伤趋于修复或肾纤维化最终结局的关键因素。
Renal tubular lesions and renal interstitial fibrosis by different causes are the common processes of chronic kidney diseases developing into end stage renal diseases. Inflammatory immune reaction has been considered as one of major pathophysiological mechanisms in the development of renal injury, which is mediated by local microenvironment. Circular injury-repair balance and disequilibrium determine whether renal tissue get repair or develop into fibrosis. Renal tubular epithelial cells (RTECs) not only are implicated in immunoregulation of renal microenvironment, but also have abundant biological functions. They play a critical role in the formation and media- tion of renal injury local microenvironment. During the beginning of renal injury and following renal repair, RTECs not only express different kinds of adhesive molecules, chemokines and mediators of inflammation to recruit foreign cells, but also can initiate and mediate local inflammatory immune reaction by transdifferentiating into immune cells or fibroblasts to undertake immune defence and injury repair or participate in immune injury due to the persistent injury factors and repair disequilibrium. Therefore RTECs might be the critical factor to determine whether renal injury get repair or develop into fibrosis.