The remodelling of blood vessels during atherosclerosis, arteriogenesis, hypertension, and varicosis is critically dependent on phenotype changes in vascular smooth muscle cells (SMC). Based on the fact that all of the aforementioned remodelling processes are basically triggered by an increase in circumferential wall strain, the aim of this study is i) to decipher the mechanism by which this biomechanical force enables the switch from a contractile to a synthetic/pro-inflammatory SMC phenotype and ii) to analyze the impact of stretch-stimulated SMC on the activity of leukocytes and the extracellular matrix during vascular remodelling. |