Uniform laminar shear stress provides a novel atheroprotective mechanism by inhibiting endothelial-to-mesenchymal transition in an ERK5-dependent manner.
EndMT modulation by shear stress is hypothesis-generating in animal models; leaves open translation to human vascular therapies.
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.
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Moonen et al. (2015) studied this question.
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