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• W1983562016 abstract "Recent evidence has demonstrated that endothelial cells can have a remarkable plasticity. By a process called Endothelial-to-Mesenchymal Transition (EndMT) endothelial cells convert to a more mesenchymal cell type that can give rise to cells such as fibroblasts, but also bone cells. EndMT is essential during embryonic development and tissue regeneration. Interestingly, it also plays a role in pathological conditions like fibrosis of organs such as the heart and kidney. In addition, EndMT contributes to the generation of cancer associated fibroblasts that are known to influence the tumor-microenvironment favorable for the tumor cells. EndMT is a form of the more widely known and studied Epithelial-to-Mesenchymal Transition (EMT). Like EMT, EndMT can be induced by transforming growth factor (TGF)-β. Indeed many studies have pointed to the important role of TGF-β receptor/Smad signaling and downstream targets, such as Snail transcriptional repressor in EndMT. By selective targeting of TGF-β receptor signaling pathological EndMT may be inhibited for the therapeutic benefit of patients with cancer and fibrosis." @default.
• W1983562016 created "2016-06-24" @default.
• W1983562016 creator A5046914597 @default.
• W1983562016 creator A5061389537 @default.
• W1983562016 date "2011-08-25" @default.
• W1983562016 modified "2023-10-09" @default.
• W1983562016 title "Regulation of endothelial cell plasticity by TGF-β" @default.
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• W1983562016 doi "https://doi.org/10.1007/s00441-011-1222-6" @default.
• W1983562016 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/3250609" @default.
• W1983562016 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/21866313" @default.
• W1983562016 hasPublicationYear "2011" @default.
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