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Proposed model: Loss of BMPR2 promotes EndMT via HMGA1. Loss of BMPR2 in PAECs leads to heightened expression of HMGA1, which increases the transcription factor Slug. HMGA1 binds to DNA and may promote binding of additional pro-EndMT transcription factors. Expression of smooth muscle genes, such as αSMA, SM22α, calponin and p-vimentin are increased and the endothelial gene PECAM1 is decreased, reflecting a mesenchymal phenotype.
