Abstract
Pulmonary artery (PA) smooth muscle cell (SMC) proliferation in response to hypoxia is a key component of the vascular remodeling that occurs in chronic hypoxic pulmonary hypertension.1,2,3 The traditional view has been that this hypoxic growth of PA SMCs is a direct consequence of sustained vasoconstriction and resulting mechanical stress, endothelial injury, and local growth factor production. Although hypoxia generally is not thought to directly promote proliferation of PA SMCs, we have discovered a novel proliferative synergism by which hypoxia could directly augment and sustain proliferative signals in the vessel wall.
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