ArticleMediators of inflammation2020
Inhibition of GPR91 Reduces Inflammatory Mediators Involved in Active Labor in Myometrium.
Article in Mediators of inflammation, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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.
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Who cites it
5 citing papers in PubMed, 5 citations in OpenAlex.
- Polysaccharides and Glycosides fromPharmaceuticals (Basel, Switzerland) · 2026Article
- Prostaglandin F2α requires activation of calcium-dependent signalling to trigger inflammation in human myometrium.Frontiers in endocrinology · 2023Article
- Targeting the succinate receptor effectively inhibits periodontitis.Cell reports · 2022Article
- CCL2: An important cytokine in normal and pathological pregnancies: A review.Frontiers in immunology · 2022Review
- Preterm Labor, a Syndrome Attributed to the Combination of External and Internal Factors.Maternal-fetal medicine (Wolters Kluwer Health, Inc.) · 2022Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
resultsGPR91 mRNA expression was significantly higher in myometrium from women during term spontaneous labor compared to no labor. Likewise, in mice, GPR91 mRNA expression was significantly upregulated in myometrium during inflammation-induced preterm labor compared to preterm no labor. In myometrial cells, IL1B and TNF significantly increased GPR91 mRNA expression. Knockdown of GPR91 by siRNA in myometrial cells significantly suppressed the secretion and/or expression of IL1B- and TNF-induced proinflammatory cytokines (GM-CSF, IL1A, IL1B, and IL6) and chemokines (CXCL8 and CCL2), myometrial contractility (expression of the contraction-associated proteins PTGFR and CX43, secretion of the uterotonic PGF
conclusionOur findings demonstrate that GPR91 is involved in the genesis of proinflammatory and prolabor mediators induced by IL1B or TNF and collectively suggest that GPR91 may contribute to augmentation of the labor processes.
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Registered trials
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