β-抑制蛋白介导的血管紧张素II受体激活促进肺动脉高压患者的肺血管重塑

2021-12-07 刘少飞 MedSci原创

AT1R β-抑制蛋白偏向激动剂可促进血管重构并使PAH恶化,这表明当前 PAH 疗法的主要益处是通过肺血管逆转重构以及血管舒张。

肺动脉高压 (PAH) 是一种与过度肺血管重塑相关的疾病,其特征是内皮细胞功能障碍和平滑肌细胞增殖,导致肺小动脉闭塞。这会导致高肺血管阻力、右心室 (RV) 肥大、扩张和最终衰竭。目前的 PAH 疗法主要针对血管活性介质,如内皮素-1 和前列环素,它们通过 G 蛋白偶联受体(如A型内皮素受体和前列环素受体)发出信号。然而,这些疗法的效用被认为是有限的,主要是作为肺血管扩张剂,不影响作为疾病进展基础的肺血管重塑。其他血管活性介质,如血管紧张素 II (AngII),也被认为与 PAH 的病理生物学有关。PAH中 AngII 和 AT 1 R的表达升高,AngII 水平升高与 PAH 进展和死亡率相关。阻塞 AT 1R 信号对 PAH 大鼠有益,包括RV 功能障碍恢复、肺血管重构减少和 PAH 进展延迟。

G 蛋白偶联受体 (GPCR),例如 AT 1R,通过异源三聚体G 蛋白和多功能 β-抑制蛋白衔接蛋白典型地发出信号,除了信号传导外,它们还促进受体内化和 G 蛋白信号传导的脱敏。随后,G 蛋白依赖性和/或 β-抑制蛋白依赖性信号通过下游介质的激活进行转导,例如 Ca 2+依赖性蛋白激酶 C 、丝裂原活化蛋白激酶信号和 GPCR介导的反式激活的受体酪氨酸激酶。G蛋白介导的AT 1R信令已被发现导致高血压,心肌肥大和心脏功能障碍,而β抑制蛋白介导的信号传导已经显示出促进心脏保护作用,并降低全身和肾血管阻力在收缩期心脏衰竭。

目前尚不清楚目前治疗的益处是否主要通过肺血管系统的血管舒张或逆转重塑介导,因为长期接受 PAH 治疗的患者仍可能出现严重的血管病变。我们假设我们可以通过使用 β-抑制蛋白偏向激动剂选择性激活 AT 1 R β-抑制蛋白介导的信号来解决这个问题,预计该激动剂可作为急性血管扩张剂同时促进 AT 1 R β-抑制蛋白-介导的信号。我们比较了偏向 β-抑制蛋白的 AT 1 R 激动剂 TRV023 与平衡激动剂AngII的生理和分子效应和拮抗剂氯沙坦治疗 PAH。我们发现偏向 β-抑制蛋白的 AT 1 R 刺激促进了肺血管重塑,表明在偏向 β-抑制蛋白的 AT 1 R 激活的情况下血管舒张会使 PAH 恶化。这些发现表明,靶向PAH 中GPCR信号传导的药物的长期有益作用不是通过血管舒张,而是通过逆转肺血管重塑。

研究总体设计:

研究结果:

β-抑制蛋白偏向的 AT 1R 激动剂的急性输注不会增加LV或RV压力;β-抑制蛋白介导的 AT 1R 激活不会改善慢性输注 PAH 大鼠的血流动力学。

阻断 β-抑制蛋白和 G 蛋白介导的 AT1R 信号可提高 MCT PAH 的存活率,β-抑制蛋白介导的 AT 1 R 信号在体内刺激细胞增殖。

AT 1 R 配体处理的 MCT 大鼠肺的RNA测序证明 TRV023 和AngII调节增殖和代谢中的重要途径

β-抑制蛋白介导的 AT 1 R 信号刺激人类 PASMC 增殖和迁移

总结:

尽管目前有治疗方法,但 PAH 是一种破坏性疾病,其预后比许多癌症都要差,3年生存率为68%至70%。因此,迫切需要新的策略来直接解决作为PAH 基础的病理性肺血管重塑。当前的 PAH 疗法,例如前列环素受体激动剂和内皮素受体拮抗剂,通过对血管平滑肌细胞的影响起到肺血管扩张剂的作用。这些药物已被证明对 PAH 有效,对运动能力和临床终点有好处; 然而,很大程度上未知这些药物的益处在多大程度上与其血管舒张或抗增殖特性相关。在这里,我们证明了作为血管扩张剂(通过阻断 G 蛋白介导的信号传导)同时通过 β-抑制蛋白促进信号传导的 AT 1 R β-抑制蛋白偏向激动剂没有有益作用并导致不利的肺血管重塑和与氯沙坦(一种阻断 G 蛋白和 β-抑制蛋白介导的信号传导的 AT 1 R 拮抗剂)相比,结局更差。不幸的是,我们无法比较这些药物对强烈 G 蛋白偏倚的 AT 1 的反应R 激动剂,此时尚未开发。同样,由于缺乏针对内皮素和前列环素受体的偏向激动剂,目前无法对这些受体进行类似的研究。由于目前没有描述的内皮素或前列环素受体上的GPCR配体偏向激动剂可以在我们的研究中进行测试,因此我们对当前 PAH 疗法的结论有限。然而,我们的研究结果表明,当前 PAH 特异性疗法的有益方面不仅是通过对血管收缩的急性作用但通过它们对肺血管重塑的长期影响。事实上,当前 PAH 疗法的有益效果很可能同时作为血管扩张剂和抗增殖剂。

 

参考文献:

Ma Z, Viswanathan G, Sellig M, Jassal C, Choi I, Garikipati A, Xiong X, Nazo N, Rajagopal S. β-Arrestin-Mediated Angiotensin II Type 1 Receptor Activation Promotes Pulmonary Vascular Remodeling in Pulmonary Hypertension. JACC Basic Transl Sci. 2021 Nov 22;6(11):854-869. doi: 10.1016/j.jacbts.2021.09.006. PMID: 34869949; PMCID: PMC8617598.

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    2021-12-08 查查佳佳

    在门诊接受治疗,但仍有部分患者重

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