Abstract

Endothelial cells (ECs), which form the inner surface of the blood vessels, contact the blood, withstand mechanical pressure, and demonstrate heterogeneous reactions to exogenous and endogenous stimuli. ECs have unique properties in accordance with their niches and play an important role in regulating vascular homeostasis. Endothelial cells may undergo a dynamic phenotypic switch in terms of its heterogeneity, which may lead to endothelial dysfunction and a number of associated pathologies. Endothelial–mesenchymal transition (EndMT) is one of the possible molecular and cellular mechanisms of this kind. EndMT is characterized by phenotypic changes in ECs through which endothelial cells acquire new properties, i.e., start producing mesenchymal markers such as alpha-SMA and vimentin, change morphology, and become able to migrate. EndMT is a complex biological process that can be induced by inflammation, hypoxia, or oxidative stress and be involved in pathogenesis of cardiovascular disease. This review describes the key markers, inhibitors, and inducers of endothelial–mesenchymal transition and overall state-of-the-art of EndMT in cardiovascular diseases.

中文翻译：

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心血管疾病中内皮-间质转化的分子和细胞方面

摘要

内皮细胞（EC）形成血管内表面，接触血液，承受机械压力，并对外源性和内源性刺激表现出异质反应。ECs 根据其生态位具有独特的特性，并在调节血管稳态中发挥重要作用。内皮细胞的异质性可能会经历动态表型转换，这可能导致内皮功能障碍和许多相关病理。内皮-间质转化（EndMT）是此类可能的分子和细胞机制之一。EndMT 的特点是 EC 发生表型变化，内皮细胞通过表型变化获得新的特性，即开始产生间充质标记物，如 α-SMA 和波形蛋白，改变形态并能够迁移。EndMT 是一个复杂的生物过程，可由炎症、缺氧或氧化应激诱导，并参与心血管疾病的发病机制。这篇综述描述了内皮-间质转化的关键标志物、抑制剂和诱导剂以及心血管疾病中 EndMT 的总体最新技术。