Commentary: Bone morphogenetic proteins contribution to pulmonary artery hypertension: Should this raise concern for patients undergoing spinal fusions with bone morphogenetic protein?

摘要

Background:Congenital pulmonary artery hypertension (PAH) has been clinically correlated in 70–80% of cases with mutations at the bone morphogenetic protein receptor 2 (BMPR2) genetic site. However, there is also clinical and basic science/laboratory literature indicating a dose–response relationship between BMP signaling and the evolution of PAH (e.g., increased endothelial, smooth muscle, and progenitor cell production, with calcifications).