Circulation:NMDA型谷氨酸受体激活可促进血管重构和肺动脉高压!

2018-06-01 MedSci MedSci原创

肺血管细胞过度增殖和凋亡抵抗是肺动脉高压(PAH)血管重构的潜在基础。现有的针对PAH的特异性治疗,大多是靶向内皮细胞功能异常,但高肺动脉压仍可导致心衰和死亡。肺动脉重构可能受血管细胞代谢重组驱动,以增加谷氨酸分解和产生。N-甲基-D-天冬氨酸受体(NMDAR),主要的神经元谷氨酸受体,也在血管细胞上表达,但其在PAH中的功能尚不清楚。Sébastien J. Dumas等人通过质谱分析、West

血管细胞过度增殖和凋亡抵抗是肺动脉高压(PAH)血管重构的潜在基础。现有的针对PAH的特异性治疗,大多是靶向内皮细胞功能异常,但高肺动脉压仍可导致心衰和死亡。肺动脉重构可能受血管细胞代谢重组驱动,以增加谷氨酸分解和产生。N-甲基-D-天冬氨酸受体(NMDAR),主要的神经元谷氨酸受体,也在血管细胞上表达,但其在PAH中的功能尚不清楚。

Sébastien J. Dumas等人通过质谱分析、Western blotting和免疫组化分析谷氨酸-NMDAR轴在PAH患者和健康对照的肺动脉中的状态。研究人员检测体外培养的肺动脉细胞释放的谷氨酸,并分析NMDAR调控/磷酸化。同时评估NMDAR封闭对人类肺动脉平滑肌细胞增殖的影响,以及NMDARs在与肺动脉高压相关的血管重构中的作用。

研究人员发现在PAH患者的肺动脉中,谷氨酸积累、NMDAR上调和NMDAR聚集(GluN1-亚基磷酸)。Kv离子通道抑制和A型选择性内膜受体激活可放大人类肺动脉血管平滑肌细胞Ca2+依赖性的谷氨酸释放,而且,A型选择性内皮细胞受体和血小板源性生长因子受体激活可导致NMDAR聚集、谷氨酸-NMDAR轴和主要的PAH相关信号通路交联增强。血小板源性生长因子-BB-诱导的人类肺动脉血管平滑肌细胞增殖涉及NMDAR激活和磷酸化的GluN1亚基定位于细胞连接,与增殖的人类肺动脉平滑肌之进行的通过NMDARs的谷氨酸交流一致。小鼠平滑肌NMDAR缺陷可减缓其由慢性缺氧触发的血管重构、增强血管NMDARs在肺动脉高压中的作用。药物阻滞肺动脉高压的大鼠模型的NMDAR对心脏和血管重构均具有保护作用,并减轻内皮细胞功能障碍、细胞增殖和凋亡抵抗,同时干扰肺动脉中的谷氨酸-NMDAR信号通路。

总而言之,本研究结果表明在PAH患者的肺动脉中,谷氨酸-NMDAR轴调节异常,提示血管NMDARs可作为PAH的抗重构治疗靶点。

原始出处:

https://doi.org/10.1161/CIRCULATIONAHA.117.029930

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    2019-04-07 wetgdt
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    2018-06-01 明天jing

    肺动脉高压表面是罕见病,事实上临床上并不少见,治疗药物虽然有一些,但是整体仍然不理解,可能未来需要采用综合治疗措施。

    0

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    2018-06-01 龙胆草

    学习谢谢分享

    0

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肺动脉高压(PAH)作为一种罕见的疾病,即使实施了特定的PAH导向疗法,依然存在预后不良的问题。最近,来自波兰的研究人员进行了一项研究,目的是根据波兰国家健康基金项目,在一个中心的患者中寻求预后不良的预测因素。

肺动脉高压 别忽视了这个少见病因

患者,男,21岁。因活动后胸闷﹑气短2年,加重并咯血4个月于2008年8月23日入院。患者2年前开始出现活动后胸闷﹑气短﹑盗汗﹑干咳等症状,曾在深圳某医院诊断为结核病,抗结核治疗半年,病情无明显好转。4个月前上述症状较前加重,活动量明显下降﹑夜间不能平卧(外院X线胸片提示肺间质性水肿)。开始出现咯血,每日2~3次,每次2~3ml,当地医院给予强心﹑利尿﹑扩血管等治疗症状好转,为进一步诊治收入我院。

Chest:系统性硬化症伴肺动脉高压患者的长期结局!

由此可见,PHAROS的总生存率高于其他SSc-PAH队列。PAH占死亡人数的一半以上,主要发生在PAH诊断后的前几年内。对于早期PAH相关性死亡风险最高的患者,优化治疗至关重要。

房间隔造口术治疗肺动脉高压 你get到了吗?

女性患者,33岁,因活动后气短、心悸,后发生咳血入院。查体见,口唇发绀,心脏扩大,第二心音亢进﹑分裂,双下肢高度水肿。经心电图、超声心动图等检查,确诊为“特发性肺动脉高压”。但经强心﹑利尿﹑扩血管﹑抗凝﹑吸氧等综合治疗后,效果不佳。遂进行房间隔球囊造口术。术后患者肺动脉压能下降到正常状态吗?血流动力学会有明显改善吗?详见以下病例。

Chest:体重指数和肥胖与肺动脉高压患者生存之间的关系!

由此可见,肥胖与总人群死亡率无关,但在年轻病态肥胖患者中年龄和肥胖与死亡率增加之间存在交互作用。这些结果对年轻的病态肥胖患者主动体重管理很有意义,而这些患者是肺脏移植的候选者。