Hypoxia and HIF activation as a possible link between sepsis and thrombosis

Thrombosis Journal

卷:17

Colin E. Evans¹ 

[1] Program for Lung and Vascular Biology, Stanley Manne Children’s Research Institute, Ann & Robert H. Lurie Children’s Hospital of Chicago;

关键词: Endothelium;    Hypoxia;    Hypoxia-inducible factors;    Integrins;    Thrombosis;   

DOI  :  10.1186/s12959-019-0205-9

来源: DOAJ

【 摘 要 】

Abstract Risk factors for thrombosis include hypoxia and sepsis, but the mechanisms that control sepsis-induced thrombus formation are incompletely understood. A recent article published in Thrombosis Journal: (i) reviews the role of endothelial cells in the pathogenesis of sepsis-associated microthrombosis; (ii) describes a novel ‘two-path unifying theory’ of hemostatic discorders; and (iii) refers to hypoxia as a consequence of microthrombus formation in sepsis patients. The current article adds to this review by describing how sepsis and thrombus formation could be linked through hypoxia and activation of hypoxia-inducible transcription factors (HIFs). In other words, hypoxia and HIF activation may be a cause as well as a consequence of thrombosis in sepsis patients. While microthrombosis reduces microvascular blood flow causing local hypoxia and tissue ischemia, sepsis-induced increases in HIF1 activation could conversely increase the expression of coagulant factors and integrins that promote thrombus formation, and stimulate the formation of pro-thrombotic neutrophil extracellular traps. A better understanding of the role of cell-specific HIFs in thrombus formation could lead to the development of novel prophylactic therapies for individuals at risk of thrombosis.

【 授权许可】

Unknown