Thus, induction of GDF-15 expression by hypoxia and shear stress in combination with its effects on cell proliferation and apoptosis suggests a functional role in pulmonary endothelial cells and thereby in the pathobiology of complex vascular lesions in pulmonary arterial hypertension (PAH) [33, 36]. However, the cellular tissue sources, as well as detailed functional effects of GDF-15 in the CVS, have not been completely elucidated. Here, GDF15 is linked to pulmonary arterial hypertension.