TY - JOUR T1 - R-克里唑替尼易患并加剧肺动脉高压的动物模型JF - 欧洲呼吸杂志JO - 欧洲呼吸j执行 - 10.1183 / 13993003.03271-2020 VL - 57 - 5 SP - 2003271 AU - Awada，Charifa AU- Grobs，Yann Au - Wu，文汇Au - Habbout，Karima Au - Romanet，Charlotte Au - Breuils-Bonnet，Sandra Au - Tremblay，Eve Au - Martineau，Sandra Au - Paulin，Roxane Au - Bonnet，SébastienAU -Provencher，Steeve Au - Potus，FrançoisAu - Boucherat，Olivier Y1 - 2021/05/01 UR - //www.qdcxjkg.com/content/57/5/2003271.abstract n2 - 肺动脉高压（pH）是一个危及生命多病因的疾病。无论潜在的原因如何，pH的特征在于肺血管壁的血管收缩和渐进式增厚，所有这些都是通过损失肺动脉内皮细胞（PAEC）[1]引发的。实际上，大量的工作表明，受损或凋亡的PAEC通过释放直接诱导收缩和增强相邻的肺动脉平滑肌细胞（PASMC）和增强抗动肌细胞（PASMC）的生存和增殖的生长，纤维和促炎因子来引发重塑过程。成纤维细胞[1,2]。在过去的十年中，激烈的研究努力旨在解读pH细胞如何获取其“癌症状”属性。因此，在临床前模型中测试了许多抗肿瘤药物的治疗潜力，其中一些致临床测定[3]。Considering the biphasic pattern of apoptosis that characterises the disease (i.e. PAEC apoptosis that triggers the disease is followed by an apoptosis-resistant state allowing vascular remodelling [4]), it is not surprising that some anticancer agents can both predispose to and treat pulmonary arterial hypertension (PAH). This is exemplified by studies showing that dasatinib, a second-generation tyrosine kinase inhibitor (TKI) approved for Philadelphia chromosome positive chronic myeloid leukaemia, improves established PAH in multiple animal models [5], while its administration before exposure to PH inducers exacerbates pulmonary vascular remodelling and pulmonary artery pressures; histological and haemodynamic changes not observed in rats exposed to dasatinib alone [6].This study demonstrates that R-crizotinib, a frontline therapy for lung cancer, predisposes to and exacerbates PH in animal models. Caution and regular follow-up should be exercised in lung cancer patients treated with the compound. http://bit.ly/39s6stp ER -