Endothelial dysfunction and thrombosis in polycythemia vera

Polycythemia vera (PV) is a chronic myeloproliferative neoplasm with an increased risk of thrombotic events. Endothelial dysfunction is a pathogenetic mechanism contributing to thrombus formation in PV. The presence of the JAK2 V617F mutation is associated with an increased risk of thrombosis due to changes in endothelial homeostasis mediated by overexpression of pro-adhesive and proinflammatory agents. Cytoreductive treatment that decreases the JAK2 allele burden and inhibits the JAK/STAT signaling pathway is potentially more effective in thrombosis prevention than drugs that are less effective in the reduction of the JAK2 allele burden. This review aims to present the spectrum of endothelial dysfunction and the impact of cytoreductive treatment on the condition of endothelial cells and thrombosis risk in patients suffering from polycythemia vera.