Key result
High shear stress suppresses pro-inflammatory endothelial signaling, potentially protecting against atherosclerosis.
Why the study?
Shear stress is believed to play a central role in regulating endothelial cell inflammatory responses and atherosclerosis pathogenesis, but the mechanisms require summarization.
This review highlights the protective, anti-inflammatory role of high shear stress on vascular endothelial cells and its implications for preventing atherosclerosis.
High shear stress anti-inflammatory effects warrant validation; leaves open specific mediators and clinical translation in atherosclerosis.
The vascular endothelium plays a pivotal role in regulating vascular homeostasis. Blood flow exerts several mechanical forces on the luminal surface of the Endothelial Cell (EC) including pressure, circumferential stretch, and shear stress. It is widely believed that shear stress plays a central role in regulating EC inflammatory responses and the pathogenesis of atherosclerosis. High shear stress can induce an antiinflammatory status in EC, which is partially mediated by the production of proteins and transcription factors able to suppress different proinflammatory signalling pathways. In this review, we summarise the available evidence regarding the effect of shear stress on vascular EC and smooth muscle cells, the regulation of MAPK and NF-κB including the production of different negative regulators of inflammation such as MKP-1 and NRF2, and the production of microRNAs. We also discuss the possible links between shear stress and the development of atherosclerosis.
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Zakkar et al. (2016) conducted a review in Atherosclerosis. Shear stress was evaluated. High shear stress induces an anti-inflammatory status in endothelial cells by suppressing pro-inflammatory signaling pathways, which may protect against the pathogenesis of atherosclerosis.
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