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Endothelium-mediated contributions to fibrosis.
Seminars in Cell & Developmental Biology ( IF 6.2 ) Pub Date : 2019-11-29 , DOI: 10.1016/j.semcdb.2019.10.015
Xuetao Sun 1 , Blessing Nkennor 2 , Olya Mastikhina 3 , Kayla Soon 3 , Sara S Nunes 4
Affiliation  

Fibrosis, characterized by abnormal and excessive deposition of extracellular matrix, results in compromised tissue and organ structure. This can lead to reduced organ function and eventual failure. Although activated fibroblasts, called myofibroblasts, are considered the central players in fibrosis, the contribution of endothelial cells to the inception and progression of fibrosis has become increasingly recognized. Endothelial cells can contribute to fibrosis by acting as a source of myofibroblasts via endothelial-mesenchymal transition (EndoMT), or by becoming senescent, by secretion of profibrotic mediators and pro-inflammatory cytokines, chemokines and exosomes, promoting the recruitment of immune cells, and by participating in vascular rarefaction and decreased angiogenesis. In this review, we provide an overview of the different aspects of fibrosis in which endothelial cells have been implicated.



中文翻译:

内皮介导的纤维化作用。

纤维化的特征是细胞外基质异常和过度沉积,从而导致组织和器官结构受损。这可能导致器官功能降低并最终导致衰竭。尽管被称为肌成纤维细胞的活化成纤维细胞被认为是纤维化的主要参与者,但内皮细胞对纤维化的发生和发展的贡献已得到越来越多的认识。内皮细胞可通过内皮-间质转化(EndoMT)充当成纤维细胞的来源,或通过衰老,分泌纤维化介质和促炎性细胞因子,趋化因子和外泌体,促进免疫细胞的募集而促成纤维化。通过参与血管稀疏和减少血管生成。在这篇评论中,

更新日期:2019-11-29
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