LAUSR

The inner lumen of the blood vessels is covered by a thin layer of cells, known as endothelial cells. The integrity of endothelial cells is important for the development of the cardiovascular system and for the protection against cardiovascular diseases. Endothelial cells have been reported to possess the ability to transdifferentiate into mesenchymal cells (endothelial-to-mesenchymal transition, EndMT) [1–3]. During the process of EndMT, endothelial cells lose their specific cell surface markers of ve-Cadherin and CD31, and instead express markers for mesenchymal or myofibroblastic cells, such as α-SMA, type I collagen, and vimentin. In this current issue of Trends in Cardiovascular Medicine, Jackson et al. [4] reviewed the signaling mechanisms and the roles of EndMT in cardiovascular development and cardiovascular pathogenesis. Here, we emphasize and further discuss the main pathways that have been implicated in both physiological and pathological EndMT. Accumulating evidence has demonstrated an intermediate role of EndMT in the embryonic development of the cardiovascular system, as discussed by Jackson et al. [4]. The authors described individual signaling pathways that have been shown to induce EndMT. Among the relevant pathways, the TGF-β/BMP and PI3K/Akt axis are particularly important, and discussed here in more detail. Endocardial suppression of TGF-β/BMP signaling by deletion of BMP receptors and Smad4, or attenuation of active Samd2/3/4 complex, resulted in a