ArticleJournal of inflammation (London, England)2025
C-reactive protein modulates lipid mediators in a pro-inflammatory direction.
Article in Journal of inflammation (London, England), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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
3 citing papers in PubMed.
- Metabolomic atlas of dengue virus infection reveals distinct circulating bioactive lipid signatures.PLoS neglected tropical diseases · 2026Article
- The CALLY index as a novel predictor of left ventricular aneurysm in patients with ST-segment elevation myocardial infarction.Frontiers in cardiovascular medicine · 2026Article
- Epicardial fat area as an independent predictor of atrial fibrillation occurrence and severity.Frontiers in cardiovascular medicine · 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
5 authors.
Funding
Abstract
backgroundC-reactive protein (CRP) is a risk factor for atherosclerosis. Although inflammation may confound this association, CRP itself has been hypothesized to possess both pro-atherosclerotic and pro-inflammatory properties. In this study, we aimed to elucidate the mechanism by which CRP may modulate bioactive lipid mediators.
resultsWe found that the overexpression of human CRP increased plasma IL-6 and TNF-a levels in mice. Moreover, the conditioned medium of CRP-overexpressing HepG2 cells increased the release of these cytokines from RAW264.7 cells to a greater degree than recombinant CRP. Lipidomics analyses then revealed that the overexpression of CRP increased the total levels of plasma lysophosphatidic acid, lysophosphatidylethanolamine, lysophosphatidylglycerol, lysophosphatidylinositol, and sphingosine 1-phosphate in mice. It also increased the levels of pro-inflammatory arachidonic acid derivatives, including PGE2 metabolites, LTA4 metabolites, and oxylipids, and decreased the levels of anti-inflammatory eicosapentaenoic acid- and docosahexaenoic acid-derived mediators. In regard to the mechanisms, analyses of CRP-overexpressing HepG2 cells suggested that CRP may increase the hepatic production of glycero-lysophospholipids, and may also modulate eicosanoids and related mediators outside the liver. Finally, analyses of the fraction separated using anti-CRP IgG suggested that CRP can bind several lipid mediators including sphingosine 1-phosphate, PGE2, and PGF2a.
conclusionsCRP may modulate lysophospholipids, and eicosanoids, and related mediators in pro-atherosclerotic and pro-inflammatory directions.
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Registered trials
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