Clin Transl Med:CD248,可能是肺动脉高压的新治疗靶点

2020-10-07 Clin Transl Med Clin Transl Med

肺动脉重塑是肺动脉高压(PAH)最重要的临床病理改变。PAH的主要表现是肺动脉平滑肌细胞(PASMCs)功能异常,导致肺动脉中层增厚和表型改变,进而动脉梗阻逐渐加重和出现右心室肥厚。据估计目前PAH在

肺动脉重塑是肺动脉高压(PAH)最重要的临床病理改变。PAH的主要表现是肺动脉平滑肌细胞(PASMCs)功能异常,导致肺动脉中层增厚和表型改变,进而动脉梗阻逐渐加重和出现右心室肥厚。据估计目前PAH在人群中的发病率为1%,在65岁以上的人群中发病率为10%,严重的PAH患者五年生存率小于60%。目前,PAH临床治疗的药物主要包括前列环素,内皮素受体拮抗剂和5型磷酸二脂酶抑制剂等。尽管如上这些治疗有一定效果,但仍不能有效地阻止PASMCs的恶性增殖和肺动脉血管的封闭性塑型。因此目前急需找到新的抗PAH肺血管重塑的靶向药。 

肺血管重塑是PAH最重要的病理特征。因为目前PAH血管重塑的机制还不十分明确,所以还没有治疗PAH的有效方法。

 2020年9月15日,Clinical and Translational Medicine杂志在线发表了锦州 Shuangyue Liu 教授团队的最新成果 “CD248 as a novel therapeutic target in pulmonary arterial hypertension”

CD248又名内皮唾酸蛋白,是一种跨膜蛋白,在周细胞和成纤维细胞中高表达。以往研究显示,CD248在健康成年人组织中表达基本消失,但在慢性纤维化疾病的基质细胞中却大量表达,且表达水平与疾病的严重程度具有相关性。敲除CD248基因序列后,组织的病理性纤维化程度明显降低。同时CD248基因的敲除能使血小板源性生长因子(PDGF)通路介导的慢性纤维化进程受到抑制,可见,CD248通过调节PDGF受体通路等跨膜转运信号通路来影响纤维化过程。因此,CD248与纤维化进程密切相关。

在本文中作者及其团队探讨了CD248在肺血管重塑中的作用以及PAH的发病机制。结果表明PASMCs中CD248激活程度与PAH的严重程度紧密相关。CD248参与了血小板来源的生长因子BB(PDGF-BB)导致的PASMC增殖和迁移,以及转化为更加明显的合成表型。相反地,如果用Cd248 siRNA或者anti-CD248治疗抗体(ontuxizumab)进行处理,可以显著地抑制PDGF信号通路, 阻断NF- κB p65介导的Nox4的转录,减少PASMCs中PDGF-BB介导的活性氧的产生。此外,knockdown CD248可以缓解PAH模型小鼠中肺血管的重塑。本项研究对PASMCs功能异常如何导致肺血管重塑进行了深入的探讨,以CD248为靶点,为PAH的抗重塑靶向治疗提供了有力的证据。

 

 

        总之,本项研究表明CD248在肺血管重塑中起关键作用。在PAH rPASMCs中CD248被上调,说明CD248参与了PASMCs的增殖和迁移过程,CD248推动了合成表型的出现和PAH疾病的进展。本项研究在PAH的抗血管重塑靶向治疗方面进行了十分深入的探索。       

 

 

原始出处:

Xu T, Shao L,Wang A, et al. CD248 as a novel therapeutic target in pulmonary arterial hypertension. Clin Transl Med . 2020;10:e175. https://doi.org/10.1002/ctm2.175.

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    2021-08-31 bsmagic9140
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    2020-10-07 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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肺动脉高压是系统性红斑狼疮严重的并发症,其特点是右心室后负荷增加,主要包括肺动脉顺应性(PAC)和肺血管阻力。PAC在预测系统性红斑狼疮相关的肺动脉高压预后中的作用尚未明确。

Circulation:MDM2介导的ACE2泛素化促进肺动脉高压进展

ACE2在Ser-680和Lys-788位点上的不适当翻译后修饰(磷酸化和泛素化)与肺动脉高压和实验性PH的发病机理有关。联合干预肺内皮细胞的AMPK和MDM2可能在PH治疗中具有一定疗效。