缺氧性肺血管收缩
钙敏感受体
血管阻力
血管收缩
缺氧(环境)
钙
肺动脉高压
生物学中的钙
细胞外
药理学
受体
医学
心脏病学
血管平滑肌
化学
内分泌学
血压
内科学
钙代谢
生物
平滑肌
细胞生物学
氧气
有机化学
作者
Jiwei Zhang,Qinli Li,Pu Liao,Rui Xiao,Li Zhu,Qinghua Hu
出处
期刊:Life Sciences
[Elsevier BV]
日期:2024-01-28
卷期号:340: 122472-122472
被引量:1
标识
DOI:10.1016/j.lfs.2024.122472
摘要
Pulmonary hypertension (PH) is characterized by elevation of pulmonary arterial pressure and pulmonary vascular resistance. The increased pulmonary arterial pressure and pulmonary vascular resistance due to sustained pulmonary vasoconstriction and pulmonary vascular remodeling can lead to right heart failure and eventual death. A rise in intracellular Ca2+ concentration ([Ca2+]i) and enhanced pulmonary arterial smooth muscle cells (PASMCs) proliferation contribute to pulmonary vasoconstriction and pulmonary vascular remodeling. Recent studies demonstrated that extracellular calcium sensing receptor (CaSR) as a G-protein coupled receptor participates in [Ca2+]i increase induced by hypoxia in the experimental animals of PH and in PH patients. Pharmacological blockade or gene knockout of CaSR significantly attenuates the development of PH. This review will aim to discuss and update the pathogenicity of CaSR attributed to onset and progression in PH.
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