ArticleMedComm2025
Persistent Activation of Sphingosine-1-Phosphate Receptor 1 by Phytosphingosine-3,4-Cyclic Phosphate Ameliorates Sepsis by Inhibiting Hyperinflammation and Vascular Hyperpermeability.
Article in MedComm, 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
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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.
- Endothelial barrier and sepsis: mechanisms and potential therapeutic strategies.Military Medical Research · 2026Review
Corrections and comments
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Authors and funding
12 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Sepsis is a life-threatening disease characterized by multiorgan dysfunction caused by an abnormal immune response to microbial infection. Sphingosine-1-phosphate (S1P) levels are significantly lower in patients with sepsis and are negatively correlated with the severity of sepsis. However, whether the S1P signaling pathway is a target for sepsis treatment remains unknown. Here, we show that our newly synthesized phytosphingosine-3,4-cyclic phosphate (3,4-cPP), a functional agonist of S1P receptor 1 (S1P1), exerts a strong protective effect against severe cecal ligation and puncture (CLP)-induced sepsis. 3,4-cPP persistently activates S1P1 without inducing internalization. 3,4-cPP upregulates SIRT1 expression in macrophages and endothelial cells via S1P1 activation. Additionally, 3,4-cPP decreases serum levels of proinflammatory cytokines, including IL-6 and TNF-α, and inhibits endothelial permeability in CLP-induced septic mice. Conditional knockout of SIRT1, an NAD
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