Pericytes and endothelial cells act as mutual, yet incomplete safeguard to sustain lung microvascular networks in pulmonary arterial hypertension

Extract Pulmonary arterial hypertension (PAH) results from extensive remodeling along the length of the arterial-to-microvascular vessel tree. Prior studies focused primarily on cellular signals driving remodeling of pulmonary arteri(ol)es in PAH. Accordingly, approved therapies target arterial vasodilation and reverse remodeling [1]. In parallel, PAH is characterized by loss (rarefaction) of pulmonary microvessels and capillaries the critical role of which is highlighted by a close correlation of vascular volume with disease severity [2].