Emerging molecular targets for anti-proliferative strategies in pulmonary arterial hypertension.

The combination of pulmonary vasoconstriction, in situ thrombosis, and pulmonary arterial wall remodeling is largely responsible for the rise in pulmonary vascular resistance (PVR) and pulmonary arterial pressure (PAP) in patients with pulmonary arterial hypertension (PAH). Even though several drugs have been developed over the past decades, at this time there is no cure for PAH. The overriding goals of the current therapeutic options seek to compensate for the defects in the relative balance of competing vasoconstrictor and vasodilator influences. Because the past decade has seen great strides in our understanding of the pathogenesis of PAH, interest has been growing in the potential use of anti-proliferative approaches in PAH. Indeed anti-proliferative strategies could offer ways not only to reinstate the homeostatic balance between cell proliferation and apoptosis but also to reverse the progressive pulmonary vascular obstruction in PAH. However, further efforts still need to be made in order to establish the long-term safety and efficacy of those anti-proliferative approaches in PAH and their potential additive benefit with other drugs.