Endothelial-to-mesenchymal transition contributes to fibro-proliferative vascular disease and is modulated by fluid shear stress

Conclusion
Together, these data suggest that EndMT contributes to neointimal hyperplasia and induces atherogenic differentiation of endothelial cells. Importantly, we uncovered that EndMT is modulated by shear stress in an ERK5-dependent manner. These findings provide new insights in the role of adverse endothelial plasticity in vascular disease and identify a novel atheroprotective mechanism of uniform LSS, namely inhibition of EndMT.

Source: Cardiovascular Research - November 17, 2015 Category: Cardiology Authors: Moonen, J.-R. A. J., Lee, E. S., Schmidt, M., Maleszewska, M., Koerts, J. A., Brouwer, L. A., van Kooten, T. G., van Luyn, M. J. A., Zeebregts, C. J., Krenning, G., Harmsen, M. C. Tags: Vascular Biology Source Type: research