In conclusion, exposure to chronic hypoxia is associated with the activation of endogenous lung angiogenic processes, which attenuate the severity of pulmonary hypertension. Recent studies also provide evidence that the angiopoietin-1/Tie2 pathway is abnormal in idiopathic PAH and contributes to PA-SMC hyperplasia through excessive release of growth factors by ECs. Since Ang1 is now considered a pericyte-derived paracrine signal for the endothelium, these findings identify dysregulation of cross-talk between endothelial and smooth muscle cells as an important component of pulmonary vascular remodeling. Further studies are needed to better understand the importance of these abnormalities in the process of hypoxia-induced smooth muscle proliferation.

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