Why the study?
There is no specific treatment for sepsis, but disturbance of the angiopoietin/Tie2 axis has been identified as a key driver of endothelial dysfunction.
The Angiopoietin/Tie2 axis is a key regulator of endothelial dysfunction in sepsis and represents a promising therapeutic target.
Disturbance of Ang/Tie2 axis may drive endothelial activation in sepsis; leaves open whether targeting it improves outcomes in trials.
Sepsis is a disorder of host response caused by severe infection that can lead to life-threatening organ dysfunction. There is no specific treatment for sepsis. Although there are many different pathogens that can cause sepsis, endothelial dysfunction is a frequent mechanism resulting in vascular leakage and coagulation problem. Recent studies on the regulatory pathways of vascular endothelium have shown that the disturbance of angiopoietin (Ang) /Tie2 axis can induce endothelial cell activation, which is the core pathogenesis of sepsis. In this review, we aim to discuss the regulation of Ang/Tie2 axis and the biomarkers involved in the context of sepsis. Also, we attempt to explore the prospective and feasibility of Ang/Tie2 axis as a potential target for sepsis intervention to improve clinical outcomes.
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Chi et al. (2024) studied this question.