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

Colin E. Evans*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

14 Scopus citations

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.

Original languageEnglish (US)
Article number16
JournalThrombosis Journal
Volume17
Issue number1
DOIs
StatePublished - Aug 14 2019

Keywords

  • Endothelium
  • Hypoxia
  • Hypoxia-inducible factors
  • Integrins
  • Thrombosis

ASJC Scopus subject areas

  • Hematology

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