ARDS 中血管生成素-2 的诅咒：在陌生的 TI(E)des 上。
The curse of angiopoietin-2 in ARDS: on stranger TI(E)des.
机构信息
Department of Medicine D, Division of General Internal Medicine, Nephrology, and Rheumatology, University Hospital Münster, Albert-Schweitzer-Campus 1, 48149, Münster, Germany.
出版信息
Crit Care. 2018 Feb 25;22(1):44. doi: 10.1186/s13054-018-1978-0.
Abstract
Pulmonary inflammation and vascular leakage are hallmarks of acute respiratory distress syndrome (ARDS), a life-threatening condition, for which there is no specific pharmacologic treatment.Recent literature suggests that leaky vessels in pulmonary infection and ARDS may be mediated through dysregulation of a non-redundant endothelial control pathway, the Tie2 receptor and its ligands, the angiopoietins.This Viewpoint summarizes results from cell-based experiments, animal models and clinical studies underlining the potential of Tie2 targeted interventions in reducing infection-mediated pulmonary hyperpermeability.
摘要
肺部炎症和血管渗漏是急性呼吸窘迫综合征（ARDS）的标志，ARDS 是一种危及生命的疾病，目前尚无特异性的药物治疗方法。最近的文献表明，肺部感染和 ARDS 中渗漏的血管可能是通过非冗余内皮控制途径 Tie2 受体及其配体血管生成素的失调来介导的。本观点总结了基于细胞的实验、动物模型和临床研究的结果，强调了靶向 Tie2 干预减少感染介导的肺高通透性的潜力。
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