提炼
我们感兴趣地阅读了文章“ CFTR受损内皮细胞的转录组分析揭示了促炎的表型” Declercq等。[1]. Cystic fibrosis transmembrane conductance regulator (CFTR) is a cyclic adenosine monophosphate (cAMP)-dependent and ATP-gated Cl-渠道和突变CFTR基因负责囊性纤维化(CF)[2]。declercq等。[1] report that CFTR impairment in endothelial cells (ECs) by CFTR silencing or inhibition (using CFTR inhibitor 172, CFTRinh-172) reduced EC proliferation, migration and autophagy. Moreover, the authors demonstrated that the loss of CFTR acts in favour of EC dysfunction characterised by pro-inflammatory phenotype favouring leukocyte extravasation. UsingCFTRknock-out (KO) mice, Declercq等。[1]发现与EC激活标记水平升高有关的肺和肝实质中的白细胞渗出增加(图1)。
抽象的
CFTR功能损失诱导内皮细胞(EC)功能障碍。肺动脉高压(PAH)患者的肺动脉ECS(PAEC)中CFTR表达降低。CFTR在PAEC中的表达丧失会导致PAH发病机理吗?https://bit.ly/3icWfa3
Footnotes
利益冲突:F。Antigny没有什么可披露的。
利益冲突:H。Le Ribeuz无话可说。
Conflict of interest: M. Humbert reports grants and personal fees from Actelion, Bayer, GSK and Acceleron, personal fees from Merck and United Therapeutics, outside the submitted work.
利益冲突:d Montani授予一个报告d personal fees from Actelion and Bayer, personal fees from GSK, Pfizer, Chiesi and Boehringer, grants, personal fees and non-financial support from MSD, non-financial support from Acceleron, outside the submitted work.
- Received2021年5月13日。
- 公认2021年5月26日。
- 版权所有©作者2021。用于复制权和权限联系权限{at} ersnet.org