High shear stress induces atherosclerotic vulnerable plaque formation through angiogenesis

Abstract

Rupture of atherosclerotic plaques causing thrombosis is the main cause of acute coronary syndrome and ischemic strokes. Inhibition of thrombosis is one of the important tasks developing biomedical materials such as intravascular stents and vascular grafts. Shear stress (SS) influences the formation and development of atherosclerosis. The current review focuses on the vulnerable plaques observed in the high shear stress (HSS) regions, which localizes at the proximal region of the plaque intruding into the lumen. The vascular outward remodelling occurs in the HSS region for vascular compensation and that angiogenesis is a critical factor for HSS which induces atherosclerotic vulnerable plaque formation. These results greatly challenge the established belief that low shear stress is important for expansive remodelling, which provides a new perspective for preventing the transition of stable plaques to high-risk atherosclerotic lesions.

p17 from HIV induces brain endothelial cell angiogenesis through EGFR-1-mediated cell signalling activation

“…There are several studies now strongly implicating 'unstable' atherosclerotic plaque thrombosis and aberrant or enhanced angiogenesis in combination with sheer stress or other risk factors 49 . Cases of acute coronary thrombosis in HIV positive individuals also occur often at young ages 50 .…”

Endothelial Glycocalyx: Novel Insight into Atherosclerosis

“…Increasing evidence suggest that high shear stress induces atherosclerotic vulnerable plaque formation through angiogenesis [46]. High shear stress can promote the growth of the collateral vessel that has stopped growing, and increase the number of the microvessel in canine myocardial infarction region [47,48].…”

“…High shear stress can promote the growth of the collateral vessel that has stopped growing, and increase the number of the microvessel in canine myocardial infarction region [47,48]. In addition, high shear stress can increase the thickness of the endodermis through anti-inflammatory reaction, inhibit the cell proliferation and promote the cell apoptosis of smooth muscle cell, might induce the expression of matrix metalloproteinases (MMPs) and the degradation of extracellular matrix [46]. Therefore, it can be speculated that low shear stress induces the initial lesion, and high shear stress promotes the formation of vulnerable plaque (Fig.…”

Atherosclerosis Treatment with Stimuli‐Responsive Nanoagents: Recent Advances and Future Perspectives

“…At the advanced stage of plaque development, the fibrous cap erodes considerably due to the increased activities of matrix metalloproteinases (MMPs), especially MMP‐2s and MMP‐9s, that can degrade extracellular matrices (ECM) . Finally, high shear stress and ECM degradation in fibrous caps induce the formation of a vulnerable plaque that is prone to rupture and can cause atherothrombosis …”