Figure 4.

Schematic representation of molecular changes induced in venous structure resulting in different biophysical properties. As previously described altered (mostly decreased) shear stress and venous hypertension are responsible for the venous wall remodeling in VVs, influencing a plethora of molecular pathways. An increased level of hydroxyproline, reduced protective endothelial glycocalyx, altered calcium signaling, imbalance in matrix metalloproteinases and their inhibitors, enhance ECM degradation and augmented nitric oxide are the most important effects described. Collectively, these alterations are responsible for modifications in collagen and elastic fibers, venous wall permeability, disrupted vessel morphology, and functioning and multiple defects associated to the progression of CVD. Legend: Up black arrow= Increased expression; Down black arrow: Decreased expression; ≠: Differential detection.