Department of Experimental Medicine and Oncology and Interuniversity Center for Hepatic Pathophysiology, University of Turin, Turin, Italy.
Antioxid Redox Signal. 2010 Jun 15;12(12):1383-430. doi: 10.1089/ars.2009.2737.
Epithelial to mesenchymal transition (EMT) is a fundamental process, paradigmatic of the concept of cell plasticity, that leads epithelial cells to lose their polarization and specialized junctional structures, to undergo cytoskeleton reorganization, and to acquire morphological and functional features of mesenchymal-like cells. Although EMT has been originally described in embryonic development, where cell migration and tissue remodeling have a primary role in regulating morphogenesis in multicellular organisms, recent literature has provided evidence suggesting that the EMT process is a more general biological process that is also involved in several pathophysiological conditions, including cancer progression and organ fibrosis. This review offers first a comprehensive introduction to describe major relevant features of EMT, followed by sections dedicated on those signaling mechanisms that are known to regulate or affect the process, including the recently proposed role for oxidative stress and reactive oxygen species (ROS). Current literature data involving EMT in both physiological conditions (i.e., embryogenesis) and major human diseases are then critically analyzed, with a special final focus on the emerging role of hypoxia as a relevant independent condition able to trigger EMT.
上皮间质转化（EMT）是一个基本过程，是细胞可塑性概念的典范，它导致上皮细胞失去极化和特化的连接结构，经历细胞骨架重组，并获得间充质样细胞的形态和功能特征。尽管 EMT 最初是在胚胎发育中描述的，在胚胎发育中，细胞迁移和组织重塑在调节多细胞生物的形态发生中起着主要作用，但最近的文献提供了证据表明，EMT 过程是一个更普遍的生物学过程，也涉及到几种病理生理状况，包括癌症进展和器官纤维化。这篇综述首先提供了一个全面的介绍，描述 EMT 的主要相关特征，然后是专门介绍那些已知调节或影响该过程的信号机制，包括最近提出的氧化应激和活性氧（ROS）的作用。然后批判性地分析了 EMT 在生理条件（即胚胎发生）和人类主要疾病中的当前文献数据，最后特别关注缺氧作为一种能够触发 EMT 的相关独立条件的新兴作用。
