Department of Medicine, Center for Vascular Biology Research, Beth Israel Deaconess Medical Center, Harvard Medical School, 330 Brookline Avenue, RN330C, Boston, MA 02215, USA.
Department of Critical Care Medicine, CRISMA Center, University of Pittsburgh, University of Pittsburgh, School of Medicine, 3347 Forbes Avenue, Suite 220, Room 202, Pittsburgh, PA 15213, USA.
Crit Care Clin. 2020 Apr;36(2):201-216. doi: 10.1016/j.ccc.2019.12.003. Epub 2020 Jan 31.
Lethal features of sepsis and acute respiratory distress syndrome (ARDS) relate to the health of small blood vessels. For example, alveolar infiltration with proteinaceous fluid is often driven by breach of the microvascular barrier. Spontaneous thrombus formation within inflamed microvessels exacerbates organ ischemia, and in its final stages, erupts into overt disseminated intravascular coagulation. Disruption of an endothelial signaling axis, the Angiopoietin-Tie2 pathway, may mediate the abrupt transition from microvascular integrity to pathologic disruption. This review summarizes preclinical and clinical results that implicate the Tie2 pathway as a promising target to restore microvascular health in sepsis and ARDS.
脓毒症和急性呼吸窘迫综合征 (ARDS) 的致命特征与小血管的健康有关。例如，肺泡中蛋白质样液体的浸润通常是由微血管屏障破裂引起的。炎症性微血管内自发血栓形成会加重器官缺血，在其最后阶段，会突然发展为明显的弥散性血管内凝血。内皮信号轴（血管生成素-Tie2 通路）的破坏可能介导了微血管完整性到病理性破坏的突然转变。这篇综述总结了临床前和临床研究结果，表明 Tie2 通路是恢复脓毒症和 ARDS 微血管健康的一个有希望的靶点。
