RESUMEN
Pulmonary artery hypertension (PAH ) is a chronic progressive disease characterized by a persistent elevation of pul-monary vascular pressure,and the disease would limit the right ventricular function severely,fail the organ and even lead to death in the end.The histopathological change of PAH is fea-tured by the restructuring of pulmonary vessels,and the abnor-mal reproduction of pulmonary artery smooth muscle cells (PASMCs)in peripheral vessels is the major pathological basis of pulmonary vascular restructuring.This paper mainly reviews the research advances on signal transduction mechanisms and their inhibitors in promoting the proliferation of pulmonary artery smooth muscle cells.
RESUMEN
Secretion of surfactant phospholipid can be stimulated by a variety of agonists acting via at least three different signal transduction mechanisms. These include the adenylate cyclase system with activation of cAMP-dependent protein kinase; activation of protein kinase C either directly or subsequent to activation of phosphoinositide-specific phospholipase C and generation of diacylglycerols and inositol trisphosphate; and a third mechanism that involves incresed Ca2+ levels and a calmodulin-dependent step. ATP stimulates secretion via all three mechanisms. The protein kinase C pathway is also coupled to phopholipase D which, acting on relatively abundant cellular phospholipids, generates diacylglycerols that further activate protein kinase C. Sustained protein kinase C activation can maintain phosphatidylcholine secretion for a prolonged period of time. It is likely that interactions between the different signaling pathways have an important role in the overall physiological regulation of surfactant secretion.