Mamazhakypov Argen, Hein Lutz, Lother Achim
Institute of Experimental and Clinical Pharmacology and Toxicology, Faculty of Medicine, University of Freiburg, Germany.
Institute of Experimental and Clinical Pharmacology and Toxicology, Faculty of Medicine, University of Freiburg, Germany; Heart Center Freiburg University, Department of Cardiology and Angiology I, Faculty of Medicine, University of Freiburg, Germany.
Pharmacol Ther. 2022 Mar;231:107987. doi: 10.1016/j.pharmthera.2021.107987. Epub 2021 Sep 1.
Pulmonary hypertension (PH) is a devastating condition characterized by pulmonary vascular remodelling, leading to progressive increase in pulmonary artery pressure and subsequent right ventricular failure. Aldosterone and the mineralocorticoid receptor (MR), a nuclear transcription factor, are key drivers of cardiovascular disease and MR antagonists are well-established in heart failure. Now, a growing body of evidence points at a detrimental role of MR in PH. Pharmacological MR blockade attenuated PH and prevented RV failure in experimental models. Mouse models with cell selective MR deletion suggest that this effect is mediated by MR in endothelial cells. While the evidence from experimental studies appears convincing, the available clinical data on MR antagonist use in patients with PH is more controversial. Integrated analysis of clinical data together with MR-dependent molecular alterations may provide insights why some patients respond to MRA treatment while others do not. Potential ways to identify MRA 'responders' include the analysis of underlying PH causes, stage of disease, or sex, as well as new biomarkers.
肺动脉高压(PH)是一种破坏性疾病,其特征为肺血管重塑,导致肺动脉压力逐渐升高,继而引发右心室衰竭。醛固酮和盐皮质激素受体(MR)作为一种核转录因子,是心血管疾病的关键驱动因素,而MR拮抗剂在心力衰竭治疗中已得到充分确立。如今,越来越多的证据表明MR在PH中发挥着有害作用。在实验模型中,药物性MR阻断可减轻PH并预防右心室衰竭。细胞选择性MR缺失的小鼠模型表明,这种效应是由内皮细胞中的MR介导的。虽然实验研究的证据似乎很有说服力,但关于MR拮抗剂用于PH患者的现有临床数据更具争议性。对临床数据与MR依赖性分子改变进行综合分析,可能有助于深入了解为何有些患者对MRA治疗有反应而另一些患者则无反应。识别MRA“反应者”的潜在方法包括分析潜在的PH病因、疾病阶段或性别,以及新的生物标志物。