2017
DOI: 10.1016/j.cytogfr.2016.09.002
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Endothelial-to-mesenchymal transition: Cytokine-mediated pathways that determine endothelial fibrosis under inflammatory conditions

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Cited by 160 publications
(158 citation statements)
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“…Numerous studies show that EndMT is regulated by some bioactive molecules, such as TGF-β, angiotensin II (AngII) and so on (Perez et al, 2017). In recent years, accumulating evidence suggests TGF-β/Smad signaling is recognized as a crucial factor involved in the process of EndMT (Kumarswamy et al, 2012; Cooley et al, 2014).…”
Section: Discussionmentioning
confidence: 99%
“…Numerous studies show that EndMT is regulated by some bioactive molecules, such as TGF-β, angiotensin II (AngII) and so on (Perez et al, 2017). In recent years, accumulating evidence suggests TGF-β/Smad signaling is recognized as a crucial factor involved in the process of EndMT (Kumarswamy et al, 2012; Cooley et al, 2014).…”
Section: Discussionmentioning
confidence: 99%
“…Subsequently, H 2 O 2 could be either reduced to a hydroxyl radical, generating a consequent increase in intracellular oxidative stress, or converted into H 2 O by catalase, thereby decreasing oxidative stress (Dröge, 2002). Accordingly, EMT, as well as endothelial-mesenchymal transition, are both stimulated by ROS (Montorfano et al, 2014; Mahalingaiah et al, 2015; Pérez et al, 2016). Increased oxidative stress creates a suitable environment for triggering mesenchymal conversion into epithelial and endothelial cells, and the induction of EMT in patients treated with PD is associated with high glucose concentrations through a mechanism mediated by ROS generation (Davies et al, 2001; Lee et al, 2004; Rhyu et al, 2005; Książek et al, 2007a,b).…”
Section: Discussionmentioning
confidence: 99%
“…During this process, epithelial cells lose expression of E-cadherin, or VE-cadherin in the case of endothelial cells, and replace them with N-cadherin. Either Ecadherin or VE-cadherin proteins are present in cellular junctions and required for cell-cell adhesion; thus, their suppression loosens cells within the epithelial or endothelial layers, allowing them to become mobile and migrate [30,31]. EndMT is also accompanied by loss of typical endothelialspecific markers, such as CD31 and vWF [30].…”
Section: Endothelial-to-mesenchymal Transitionmentioning
confidence: 97%
“…EndMT is also accompanied by loss of typical endothelialspecific markers, such as CD31 and vWF [30]. The downregulation of endothelial properties is followed by upregulation of genes characteristic of mesenchymal cells such as SMA, Vimentin, Periostin, FSP-1, and PDGFRα/β as well as reorganization of the cytoskeleton that transforms endothelial cells to fibroblast-like cells [30]. The initial EndMT step of downregulation of cadherin expression is accomplished by a number of transcriptional repressors such as Snail, Twist and Slug [32][33][34].…”
Section: Endothelial-to-mesenchymal Transitionmentioning
confidence: 98%
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