Emerging roles of inflammation-mediated endothelial-mesenchymal transition in health and disease.
Emerging roles of inflammation-mediated endothelial-mesenchymal transition in health and disease.
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DOI：
10.1186/s41232-021-00186-3
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发表时间：
2022-02-07
影响因子：
8.1
通讯作者：
Watabe T
中科院分区：
文献类型：
--
作者：
Yoshimatsu Y;Watabe T
内皮-间充质转化（EndoMT）是内皮细胞（ECs）失去其特性并向间充质细胞分化的细胞分化过程，不仅在发育过程中被观察到，而且在成人的各种病理状态中也被观察到，包括癌症进展和器官/组织纤维化。转化生长因子-β (TGF-β)是一种炎症相关的细胞因子，已被证明在诱导EndoMT中发挥核心作用。TGF-β通过调节各种转录因子、信号分子和赋予内皮细胞间质特性的细胞成分的表达诱导EndoMT。然而，TGF-β本身并不一定足以诱导EndoMT，从而使EndoMT相关疾病的进展达到难治性程度。除了TGF-β外，通常还需要其他炎症因子的额外激活来稳定EndoMT的进展。由于最近的证据表明炎症信号分子作为EndoMT的增强剂，我们总结了炎症因子在诱导EndoMT和相关疾病中的作用。我们希望这篇综述将有助于制定针对炎症介导的EndoMT相关疾病的治疗策略。
Endothelial–mesenchymal transition (EndoMT), a cellular differentiation process in which endothelial cells (ECs) lose their properties and differentiate into mesenchymal cells, has been observed not only during development but also in various pathological states in adults, including cancer progression and organ/tissue fibrosis. Transforming growth factor-β (TGF-β), an inflammation-related cytokine, has been shown to play central roles in the induction of EndoMT. TGF-β induces EndoMT by regulating the expression of various transcription factors, signaling molecules, and cellular components that confer ECs with mesenchymal characteristics. However, TGF-β by itself is not necessarily sufficient to induce EndoMT to promote the progression of EndoMT-related diseases to a refractory extent. In addition to TGF-β, additional activation by other inflammatory factors is often required to stabilize the progression of EndoMT. Since recent lines of evidence indicate that inflammatory signaling molecules act as enhancers of EndoMT, we summarize the roles of inflammatory factors in the induction of EndoMT and related diseases. We hope that this review will help to develop therapeutic strategies for EndoMT-related diseases by targeting inflammation-mediated EndoMT.
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影响因子：
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