间充质干细胞促进肾脏缺血再灌注损伤修复机制的研究进展  

Mechanism for promoting repair of renal ischemia reperfusion injury by mesenchymal stem cells

作　　者：陶于洪[1] 叶丽[1] 王亚妹[1] 王峥[1] 

机构地区：[1]四川大学华西第二医院儿科,四川成都610041

出　　处：《中国当代儿科杂志》2013年第2期157-160,F0003,共5页Chinese Journal of Contemporary Pediatrics

摘　　要：临床前研究证实,外源性间充质干细胞(MSCs)能够改善肾脏缺血再灌注损伤的肾损害和促进肾脏修复。本文着重讨论MSCs促进肾脏缺血再灌注损伤修复机制。MSCs向缺血后肾脏靶向归巢与MSCs表达CX-CR4和CD44等趋化因子受体有关。MSCs直接分化为肾小管上皮细胞并非MSCs促进肾脏修复的主要机制。更主要的是,MSCs将通过旁分泌机制,分泌一系列的细胞因子和释放微泡,发挥激活肾内细胞、促进血管生成、抑制氧化应激、抗凋亡、抗炎和抗纤维化等效应,从而促进肾脏缺血再灌注损伤修复。Preclinical studies have demonstrated that exogenous mesenchymal stem cells （MSCs） may ameliorate kidney damage and enhance repair of renal ischemia reperfusion injury（IRI）. This review will focus on the mechanism for accelerating repair of renal IRI by MSCs. Several chemokine receptors such as CXCR4 and CD44 are related to MSCs trafficking to post-ischemic kidney. MSCs differentiate into tubular epithelial cells, which is not the predominant mechanism for repair of the damaged kidney. Instead, MSCs exert their therapeutic effect mainly through paracrine action via a variety of cytokines and microvesicles, and the paracrine actions of infused MSCs work to activate intrinsic kidney cells, promote angiogenesis, inhibit uxidative stress and reduce apoptosis, inflammation and renal fibrosis.

关 键 词：肾脏 缺血再灌注损伤 归巢 分化 旁分泌 间充质干细胞 

分 类 号：R329[医药卫生—人体解剖和组织胚胎学]