plasma levels of serotonin, which promotes vasoconstriction, hypertrophy and proliferation, are increased in patients with pah, although the role played by serotonin in the pathogenesis of pah remains uncertain. the expression or activity of several growth factors (including platelet-derived growth factor, basic fibroblast growth factor, epidermal growth factor, and vascular endothelial growth factor) is increased and contributes to vascular remodeling in pah. other factors underlying the proliferative state of pulmonary vascular smooth muscle cells include opg and trail. focusing only on the pulmonary vasculature provides an incomplete picture of pah; the ability of the right ventricle to adapt to the increased workload varies between patients and is an important determinant of survival. the molecular pathology of pah in the right ventricle is therefore also being investigated, and recent research has shifted to consider the cardiopulmonary unit as a single system rather than two separate systems. importantly, right ventricular remodeling is associated with increased apoptosis; this is in contrast to pulmonary vascular remodeling which involves inhibition of apoptosis.