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. Author manuscript; available in PMC: 2016 Feb 27.
Published in final edited form as: Circ Res. 2015 Jan 13;116(5):857–866. doi: 10.1161/CIRCRESAHA.116.305629

Figure 6. BMP7 inhibits EndMT induced by different pathways.

Figure 6

(A) Schematic representation of EndMT regulated by different signaling pathways. Extrinsic signals stimulate endothelial cells to undergo EndMT through ligands binding to various receptors such as receptor tyrosine kinases (RTK), transforming growth factor receptor (TGFBR), and NOTCH receptor. Once getting activated, these pathways either independently trigger unknown mechanisms or work in concert through common pathway intermediates like SMAD2/3, thereby activating EndMT transcription factor, which leads to loss of endothelial cell characteristics, i.e. expression of VE-Cadherin. The presence of BMP7 can activate the BMP pathway through binding to bone morphogenetic protein receptors (BMPR), thereby activating SMAD1/5/8 which can block the EndMT-inducing signals to ultimately maintain endothelial cell characteristics.