Lai Ning, Lu Wenju, Wang Jian
State Key Laboratory of Respiratory Diseases, Guangzhou Institute of Respiratory Disease, The First Affiliated Hospital of Guangzhou Medical University China.
Int J Clin Exp Pathol. 2015 Feb 1;8(2):1081-92. eCollection 2015.
Alveolar hypoxia, a consequence of many lung diseases, can have adverse effects on the pulmonary vasculature. The changes that occur in the pulmonary circulation with exposure to chronic hypoxia include reductions in the diameter of the pulmonary arteries due to structural remodeling of the vasculature. Although the structural and functional changes that occur in the development of pulmonary hypertension have been well investigated, less is known about the cellular and molecular mechanisms of this process. This review will discuss the role of several potassium and calcium channels in hypoxic pulmonary vasoconstriction, both in elevating calcium influx into pulmonary artery smooth muscle cells (PASMCs). In addition to other signal transduction pathways, Ca(2+) signaling in PASMCs plays an important role in the development and progression of pulmonary hypertension due to its central roles in vasoconstriction and vascular remodeling. This review will focus on the effect of chronic hypoxia on ion channels and the potential pathogenic role of Ca(2+) signaling and regulation in the progression of pulmonary hypertension.
肺泡缺氧是许多肺部疾病的后果,可对肺血管系统产生不利影响。长期暴露于低氧环境下,肺循环中发生的变化包括由于血管结构重塑导致肺动脉直径减小。尽管肺动脉高压发展过程中发生的结构和功能变化已得到充分研究,但对这一过程的细胞和分子机制了解较少。本综述将讨论几种钾通道和钙通道在低氧性肺血管收缩中的作用,二者均会增加钙流入肺动脉平滑肌细胞(PASMCs)。除其他信号转导途径外,PASMCs中的Ca(2+)信号传导因其在血管收缩和血管重塑中的核心作用,在肺动脉高压的发生和发展中起重要作用。本综述将重点关注慢性缺氧对离子通道的影响以及Ca(2+)信号传导和调节在肺动脉高压进展中的潜在致病作用。