Key result
Various molecules associated with vascular permeability in sepsis, such as VEGF, angiopoietin, and sphingosine-1-phosphate, are expected to become targets for clinical treatment.
Why the study?
Factors and mediators regulating vascular permeability in sepsis may become therapeutic targets for clinical treatment.
This review highlights key molecular targets regulating vascular permeability in sepsis, which may serve as potential therapeutic targets for preventing septic shock and multiple organ dysfunction syndrome.
These associations remain hypothesis-generating in sepsis; should not change practice until validated in trials.
Sepsis is one of the critical illnesses caused by burns, trauma, shock, infection, and so on. In patients with sepsis, vascular permeability is prone to develop through various pathophysiological mechanisms and thus could result in accumulation of tissue fluid, insufficient intravascular fluid, and finally cause septic shock and multiple organ dysfunction syndrome. Recent studies have shown that various factors and mediators involved in the regulation of vascular permeability in sepsis are expected to become targets for clinical treatment of sepsis. In this paper, we have reviewed the research advances on some molecules which are significantly associated with vascular permeability in sepsis, such as vascular endothelial growth factor, angiopoietin, sphingosine-1-phosphate, heparin-binding protein, and Slit2.
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He et al. (2020) conducted a review in Sepsis. Molecular mechanisms of vascular permeability (e.g., VEGF, angiopoietin, S1P, HBP, Slit2) was evaluated. Various molecules associated with vascular permeability in sepsis, such as VEGF, angiopoietin, and sphingosine-1-phosphate, are expected to become targets for clinical treatment.
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