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）是一种以肺血管重塑为特征的破坏性疾病，导致肺动脉压力进行性增加和随后的右心室衰竭。醛固酮和盐皮质激素受体 (MR) 是一种核转录因子，是心血管疾病的关键驱动因素，而 MR 拮抗剂在心力衰竭中得到广泛应用。现在，越来越多的证据表明 MR 在 PH 中的有害作用。在实验模型中，药理学 MR 阻断减弱了 PH 并防止了 RV 衰竭。具有细胞选择性 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。虽然来自实验研究的证据似乎令人信服，但关于 PH 患者使用 MR 拮抗剂的现有临床数据更具争议性。临床数据的综合分析与 MR 依赖的分子改变可能会提供一些见解，为什么有些患者对 MRA 治疗有反应，而另一些则没有。识别 MRA“反应者”的潜在方法包括分析潜在的 PH 原因、疾病阶段或性别，以及新的生物标志物。