ReviewJournal of cellular and molecular medicine2025
Role of Tie-2 Axis in Sepsis: A Potential Therapeutic Target.
Review in Journal of cellular and molecular medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed.
- Modulation of the Receptor Tyrosine Kinase TIE2/International journal of molecular sciences · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
Abstract
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.
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Identifiers
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.