Abstract
We read with interest the recent article “Mechanical Activation of Hypoxia-Inducible Factor 1α Drives Endothelial Dysfunction at Atheroprone Sites” in which Feng et al1 elegantly show that exposure of endothelial cells to mechanical low shear stress activates hypoxia-inducible factor 1α (HIF-1α). Because atherosclerosis develops near branches or bends of arteries where endothelial cells are exposed to low shear stress, these results suggest that HIF-1α activation in endothelial cells may play a causal role in the pathogenesis of atherosclerosis. Feng et al showed that upregulation of HIF-1α occurs via a dual mechanism involving transcriptional activation by nuclear factor-κB (NF-κB) and stabilization via the deubiquitinating enzyme Cezanne. We were pleased to see that the study by Feng et al1 largely recapitulated our recently published findings. In our study,2 we took an unbiased approach and performed RNAseq in human arterial endothelial cells (ECs) exposed to either unidirectional flow (atheroprotective hemodynamics of high shear …
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