Varicose veins: role of mechanotransduction of venous hypertension

Abstract

Varicose veins affect approximately one-third of the adult population and result in significant psychological, physical, and financial burden. Nevertheless, the molecular pathogenesis of varicose vein formation remains unidentified. Venous hypertension exerted on veins of the lower extremity is considered the principal factor in varicose vein formation. The role of mechanotransduction of the high venous pressure in the pathogenesis of varicose vein formation has not been adequately investigated despite a good progress in understanding the mechanomolecular mechanisms involved in transduction of high blood pressure in the arterial wall. Understanding the nature of the mechanical forces, the mechanosensors and mechanotransducers in the vein wall, and the downstream signaling pathways will provide new molecular targets for the prevention and treatment of varicose veins. This paper summarized the current understanding of mechano-molecular pathways involved in transduction of hemodynamic forces induced by blood pressure and tries to relate this information to setting of venous hypertension in varicose veins.

Figure 1

Diagram showing foot venous pressure during exercise in the standing position. Lower curve illustrates normal venous pressure while upper curve shows venous pressure in patients with venous reflux.

Figure 2

Mechanosensors of circumferential stretch in ECs. Information is compiled for both arterial and venous ECs due to scarcity of studies on venous ECs. Not all ion channels are included. This illustration is not drawn to scale.

Figure 3

Signaling pathways of varicose vein formation.