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


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
Issue number1
StatePublished - Aug 14 2019


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

ASJC Scopus subject areas

  • Hematology


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