Circulation:表观调控因子TET2或可作为肺动脉高压的生物标志物

2020-06-16 QQY MedSci原创

肺动脉高压(PAH)是一种致命的血管病。遗传病例与BMPR2及其他16个基因的胚系突变相关;但这些突变发生在不到25%的特发性PAH患者中,在结缔组织疾病相关的PAH中很少见。临床前研究表明表观遗传失

肺动脉高压(PAH)是一种致命的血管病。遗传病例与BMPR2及其他16个基因的胚系突变相关;但这些突变发生在不到25%的特发性PAH患者中,在结缔组织疾病相关的PAH中很少见。临床前研究表明表观遗传失调,包括DNA甲基化改变,可促进PAH。Tet-甲基胞嘧啶-双加氧酶-2(TET2)是DNA脱甲基化的关键酶,其体细胞突变可见于心血管疾病,并与克隆性造血、炎症和不良血管重塑有关。但TET2 在PAH中的作用尚不明确。

为了研究TET2在PAH中的作用,Potus等人对来自PAH生物库的2572例病例进行研究。在该队列中,采用1832例非亲缘的欧洲PAH患者进而7509例非芬兰欧洲个体(作对照)来检测基因特异性的罕见变异的相关性。在一个包含140位患者的独立队列中,研究人员定量检测了TET2在外周血单核细胞中的表达水平。

研究结果显示,与对照相比,PAH患者的罕见、预测的有害胚系突变的负荷增加(9/1832 vs 6/7509;相对风险=6;P=0.00067)。在整个队列中,0.39%的患者(10/2572)携带了12个TET2突变(75%为胚系,25%为体细胞突变)。这些患者不携带其他PAH相关基因突变。携带TET2突变的患者年龄更大(71±7 vs 48±19岁; P<0.0001),对血管扩张剂刺激无应答可能性更高(0/7 vs 140/1055 [13.2%]),肺血管阻力较低(5.2±3.1 vs 10.5±7.0; P=0.02),炎症增加(包括IL-1β升高)。循环TET2表达水平与年龄无关,在PAH患者中的表达量减少了86%以上。Tet2敲除小鼠自发进展成PAH,不良肺血管重构和炎症,且伴有细胞因子水平升高,包括IL-1β。长期予以靶向IL-1β的抗体进行阻断可诱导PAH消退。

PAH是第一种与潜在的TET2胚系突变相关的人类疾病。TAE2的遗传性和获得性变异见于0.39%的PAH病例。TET2表达降低在PAH中普遍存在,或有可能作为PAH的生物标志物.

原始出处:

Novel Mutations and Decreased Expression of the Epigenetic Regulator TET2 in Pulmonary Arterial Hypertension. Circulation. 2020;141:1986–2000

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    2021-05-01 yhy100200
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    2020-06-18 neurowu
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    2020-06-16 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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