University Health Network-Toronto General Hospital, Toronto, ON, Canada.
Virulence. 2013 Aug 15;4(6):572-82. doi: 10.4161/viru.25740. Epub 2013 Jul 16.
Recent evidence suggests that loss of endothelial barrier function and resulting microvascular leak play important mechanistic roles in the pathogenesis of infection-related end-organ dysfunction and failure. Several distinct therapeutic strategies, designed to prevent or limit infection-related microvascular endothelial activation and permeability, thereby mitigating end-organ injury/dysfunction, have recently been investigated in pre-clinical models. In this review, these potential therapeutic strategies, namely, VEGFR2/Src antagonists, sphingosine-1-phosphate agonists, fibrinopeptide Bβ 15-42, slit2N, secinH3, angiopoietin-1/tie-2 agonists, angiopoietin-2 antagonists, statins, atrial natriuretic peptide, and mesenchymal stromal (stem) cells, are discussed in terms of their translational potential for the management of clinical infectious diseases.
最近的证据表明，内皮屏障功能的丧失和由此导致的微血管渗漏在感染相关的终末器官功能障碍和衰竭的发病机制中起着重要的作用。最近已经在临床前模型中研究了几种不同的治疗策略，旨在预防或限制感染相关的微血管内皮激活和通透性，从而减轻终末器官损伤/功能障碍。在这篇综述中，讨论了这些潜在的治疗策略，即 VEGFR2/Src 拮抗剂、鞘氨醇-1-磷酸激动剂、纤维蛋白肽 Bβ 15-42、slit2N、secinH3、血管生成素-1/tie-2 激动剂、血管生成素-2 拮抗剂、他汀类药物、心房利钠肽和间充质基质（干）细胞，根据它们在治疗临床感染性疾病方面的转化潜力进行了讨论。
