Mouratoglou Sophia-Anastasia, Giannakoulas George, Deftereos Spyridon, Giannopoulos Georgios, Angelidis Christos, Cleman Michael W, Vassilikos Vassilios P
Third Department of Cardiology, Ippokrateio General Hospital, Medical School, Aristotle University of Thessaloniki, Konstantinoupoleos 49, 54642, Thessaloniki, Greece.
Med Chem. 2016;12(2):162-9. doi: 10.2174/157340641202160209095051.
Pulmonary arterial hypertension (PAH) is a serious life threatening disease that leads to right heart failure and death. Elevated pulmonary vascular resistance (PVR) is the main pathophysiological component that leads to elevated pulmonary arterial pressures and increased right ventricular afterload. Increased PVR is related to different mechanisms that include vasoconstriction, proliferative and obstructive remodeling of the pulmonary vessel wall and in situ thrombosis. Numerous molecular, genetic and humoral abnormalities have been proposed to play an important role in pulmonary vasoconstriction and remodeling. Of those, calcium (Ca(+2)) is a well recognized parameter involved in the pathogenetic mechanisms of PAH, because of its twofold role in both vasoconstriction and pulmonary artery smooth muscle cell (PASMC) proliferation. The aim of this review is to focus on Ca(+2) handling and dysregulation in PASMC of PAH patients.
肺动脉高压（PAH）是一种严重的、危及生命的疾病，可导致右心衰竭和死亡。肺血管阻力（PVR）升高是导致肺动脉压力升高和右心室后负荷增加的主要病理生理因素。PVR升高与多种机制有关，包括血管收缩、肺血管壁的增殖性和阻塞性重塑以及原位血栓形成。许多分子、遗传和体液异常被认为在肺血管收缩和重塑中起重要作用。其中，钙（Ca(+2)）是PAH发病机制中一个公认的参数，因为它在血管收缩和肺动脉平滑肌细胞（PASMC）增殖中都具有双重作用。本综述的目的是聚焦于PAH患者PASMC中的钙（Ca(+2)）处理及失调情况。
