钙库操纵性钙通道特性及其与低氧性肺血管收缩、重构的关系

Characteristics of store-operated channels and its effect on hypoxic pulmonary vasoconstriction and remodeling

肺动脉平滑肌细胞内Ca^2＋浓度增加是导致低氧性肺血管收缩与重构的重要分子基础。由瞬时受体电位蛋白构成的钙库操纵性钙通道（store-operated channels，SOC）是调节细胞内Ca^2＋浓度的重要机制，并参与了肺动脉高压时血管收缩和重构过程。充分了解SOC通道的特性，对深入认识肺动脉高压发病的病理生理学机制、指导临床治疗策略具有重要意义。

Enhancement of cytosolic free Ca^2＋ concentration in pulmonary arterial smooth muscle cells plays a vital role in hypoxic pulmonary vasoconstriction and remodeling. Transient receptor potential proteinencoded store-operated channels （SOC） are important to mediate Ca^2＋ influx in most cells. In pulmonary artery hypertension, SOC participate in the process of pulmonary vascular constriction and remodeling. Research of characteristics of SOC is meaningful in pathogenetic mechanism and clinical treatment strategy of pulmonary artery hypertension.