摘要
肾纤维化是慢性肾脏病进展至终末期的共同表现,已有研究显示,内皮细胞(ECs)结构功能异常是促进肾纤维化进展的重要因素。ECs在TGF-β、Notch、Wnt以及miRNAs等多种信号通路和分子作用下可发生内皮间质转化(EndMT)。EndMT一方面诱发ECs功能障碍,导致肾组织缺氧;另一方面通过旁分泌作用引起肌成纤维细胞以及肾小管上皮细胞功能异常,促进肾纤维化进展。阻断EndMT可降低肌成纤维细胞活化程度,改善组织缺氧,从而延缓肾纤维化进程。本文就EndMT在肾纤维化中的作用及其调控机制的研究进展进行阐述,以期为治疗肾纤维化提供新的靶点和策略。
Renal fibrosis is a common manifestation of chronic kidney disease progressing to the end stage.Previous studies have shown that the structural and functional abnormalities of endothelial cells(ECs)are important factors in promoting the progression of renal fibrosis.ECs can undergo endothelial-to-mesenchymal transition(EndMT)regulated by various signaling pathways and molecular actions,such as TGF-β,Notch,Wnt and miRNAs.On the one hand,EndMT induces ECs dysfunction,leading to kidney hypoxia.On the other hand,EndMT can cause abnormal changes in the function of the myofibroblasts and renal tubular epithelial cells through paracrine factors,and promote the renal fibrosis progression.EndMT blockade can reduce the degree of myofibroblasts activation and improve hypoxia,thereby alleviating the renal fibrosis progression.In this review,we summarize the research progress of the functions and mechanisms of EndMT in renal fibrosis in order to provide new targets and strategies for the treatment of renal fibrosis.
作者
张小燕
王若楠
孙嘉星
丰星星
梁亮
韩骅
刘晓渭
晏贤春
ZHANG Xiaoyan;WANG Ruonan;SUN Jiaxing;FENG Xingxing;LIANG Liang;HAN Hua;LIU Xiaowei;YAN Xianchun(Department of Nephrology,Xijing HospitalXijing Hospital,Air Force Medical University,Xi'an 710032,China;Department of Biochemistry and Molecular Biology,School of Basic Medical SciencesXijing Hospital,Air Force Medical University,Xi'an 710032,China;State Key Laboratory of Cancer BiologyXijing Hospital,Air Force Medical University,Xi'an 710032,China;Department of Ophthalmology,Xijing Hospital,Air Force Medical University,Xi'an 710032,China)
出处
《空军军医大学学报》
CAS
2022年第3期359-364,共6页
Journal of Air Force Medical University
基金
国家自然科学基金(31730041,31671523,82003110)
陕西省自然科学基金(2020JQ-441)
肿瘤生物学国家重点实验室自主课题(CBSKL2019ZZ25)。
