InSilc vitro cell models

Following drug-eluting BVS deployment, a strong healing response may initiate within the arterial wall, producing a renarrowing of the vessel due to migration and proliferation of medial VSMCs towards the vessel lumen 125, 126. The mechanical stress, generated during the expansion of the drug-eluting BVS could cause injury to the artery, which leads to thrombosis formation in the arterial wall and a cascade of inflammatory events. The in-vivo injury of vessel leads to the activation of VSMCs, which from a quiescent and contractile phenotype in the uninjured artery assumed a synthetic phenotype. This change of phenotype is followed by migration and proliferation of dedifferentiated VSMCs towards the lumen and lesion formation 127, 128, 129. Several factors are involved in the modulation of VSMC phenotype from a quiescent to a synthetic phenotype, including endothelial damage and denudation during drug-eluting BVS deployment: these factors could produce adhesion of thrombocytes that express mitogenic chemokines, resulting in the chemotactic migration and proliferation of VSMCs towards the lumen. Although there have been extensive studies on the roles of growth factors, cytokines and inflammatory factors in the development of atherosclerosis and restenosis, the effects of hemodynamic forces, especially fluid shear stress, on the phenotype of SMCs are less well understood.