Molecular basis of cardiac endothelial-to-mesenchymal transition (EndMT): Differential expression of microRNAs during EndMT

► A small molecule inhibitor of TβRI-kinase (prevents Smad phosphorylation and activation), but not MEK inhibitor (prevents ERK phosphorylation), blocks cardiac endothelial-to-mesenchymal transition (EndMT) ► The epigenetic regulator ATp300 is significantly elevated during cardiac EndMT ► Several miRNAs, the epigenetic regulators, are differentially regulated during cardiac EndMT. The level of cellular p53, a target of miR-125b, is downregulated during EndMT ► Epigenetic regulators, specific miRNA and ATp300, may be an ideal target to controlling cardiac EndMT and EndMT-derived fibroblast-like cells-contributed cardiac fibrosis