中文摘要：

内皮间质转化是上皮间质转化的一种,是新近发现的一种细胞转化类型,和上皮间质转化一样也参与体内各种病理生理过程。已经证实,在转化过程中内皮细胞首先发生细胞与细胞脱联系过程,失去内皮细胞特异性标志物CD31和VE-钙粘蛋白,获得间质细胞特异性标志物α-SMA和FSP1,由原来的鹅卵石样结构转变为细长梭形结构,同时其迁移力和侵袭力明显增强。早期研究显示内皮间质转化在胚胎期心内膜的发育中发挥了十分关键的作用。近些年来,人们逐渐认识到内皮间质转化也参与各种疾病的发生发展,包括心、肺、肾等重要器官纤维化、特发性门脉高压、动脉粥样硬化、肺动脉高压以及肿瘤等。转化生长因子-β、Notch信号、Wnt信号以及MicroRNAs等参与对内皮间质转化的调节,然而,其具体机制尚未完全明确。通过探索内皮间质转化过程中重要信号通路及各因子的作用机制,可能为多种疾病的预防和治疗提供新的指导意见。

英文摘要：

Endothelial-mesenchymal transition （EndMT）, a newly recognized type of cellular transition, is a specific form of epithelial-mesenchymal transition, and has been demonstrated to participate in biological and pathological process. This so-called mesenchymal phenotype can be characterized by loss of cell-cell junctions, acquisition of highly invasive and migratory properties, loss of endothelial specific markers, such as CD31 （also known as platelet endothelial cell adhesion molecule-l, PECAM-1）and VE-cadherin, and gain of mesenchymal markers, such as fibroblast-specific protein 1 （FSP1, also known as S100A4） or a-smooth muscle actin （et-SMA）, alteration in cytoskeletal composition and organization to induce a striking change in cell morphology that forms elongated, sp- indle-shaped cells. Previous studies showed that EndMT was a critical process of embryonic cardiac development. Emerging evidence in recent years shows, endothelial-mesenchymal transition participate in a number of diseases ,including pulmonary, intestinal ,cardiac,and kidney fibrosis, idiopathic portal hypertension, atherosclerosis, pulmonary hypertension, tumors and so forth. However, little is known about the signaling mechanisms that cause endothelial cells to transform into mesenehymal cells. Transforming growth factor-β, Notch, Wnt, microRNAs or other signaling pathways and cytokines could direct or interact to mediate EndMT. Therefore, to address its potential mechanisms of EndMT may provide novel therapeutic strategies for treating diseases.