Role of Tie-2 Axis in Sepsis: A Potential Therapeutic Target

The angiopoietins (Angs)-Tie-2 axis initiates signalling pathways that modulate vascular stability and angiogenesis and plays an important role in a variety of physiological and pathological processes, including inflammation, wound healing and cancer, by regulating endothelial cell proliferation, survival, migration, invasion and/or differentiation. Disruption of Ang-1/2 and the Tie-2 receptor can lead to endothelial cell activation or dysfunction, which can contribute to the pathogenesis of sepsis. Although the mechanisms by which the Ang-Tie-2 axis participates in sepsis pathogenesis have not been fully elucidated due to the dynamic and complicated nature of sepsis, Ang-Tie-2 axis malfunction causes endothelial cell activation and contributes to sepsis pathogenesis. During the initiation and development of sepsis, endothelial cells secrete Ang-2, which inhibits Tie-2 activation and subsequent signalling, leading to endothelial damage, increased vascular permeability, exacerbated inflammation and multiorgan injury. In this review, we summarise the latest advances in basic and clinical research on relevant papers from the PubMed database. We aim to offer a comprehensive overview of the current state of the art of the Ang-Tie-2 axis in the context of sepsis and to explore the potential therapeutic targets for treating sepsis. A better understanding of the regulatory mechanisms related to the Ang-Tie-2 axis could help identify potential therapeutic targets for treating sepsis.