Current advances in the pathogenesis of varicose veins.

Varicose veins have a wide prevalence and are characterized by their tortuous, dilated, and serpentine appearance. This pattern is the result of disruption of the normal arrangement of the extracellular matrix (ECM) and smooth muscle cells (SMC) in veins. Valvular incompetence and the effect of increased hydrostatic pressure have been implicated in the pathogenesis of varicose veins. Alterations in the ECM and varied expression of metalloproteinases and their inhibitors can effect changes in venous wall remodeling. Gene expression and specific candidate markers have been identified in varicose veins. Differential gene transcription may influence the adaptive response of the venous wall to stimuli and the remodeling of the ECM that leads to the development of varicose veins.