ArticleJournal of endometriosis2011
Inhibition of macrophage migration inhibitory factor reduces endometriotic implant size in mice with experimentally induced disease.
Article in Journal of endometriosis, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 1 of them a synthesis that pooled it.
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
11 citing papers in PubMed, 1 synthesis or guideline pooled it, 15 citations in OpenAlex.
- Pharmaceuticals targeting signaling pathways of endometriosis as potential new medical treatment: A review.Medicinal research reviews · 2021Pooled it
- 2-Deoxyglucose Dendrimer-Enabled Niclosamide Delivery to FRβ-Expressing Macrophages Alleviates Endometriosis Progression and Associated Hyperalgesia.Advanced healthcare materials · 2026Article
- 2-Deoxyglucose dendrimer-enabled niclosamide delivery to FRβ-expressing macrophages alleviates endometriosis progression and associated hyperalgesia.bioRxiv : the preprint server for biology · 2026Article
- Multiple lesion inductions intensify central sensitization driven by neuroinflammation in a mouse model of endometriosis.bioRxiv : the preprint server for biology · 2025Article
- Targeting the CD74 signaling axis suppresses inflammation and rescues defective hematopoiesis inScience translational medicine · 2025Article
- Dissecting theBiomedicines · 2022Article
- Macrophage Migration Inhibitory Factor Receptor, CD74, is Overexpressed in Human and Baboon ( Papio Anubis) Endometriotic Lesions and Modulates Endometriotic Epithelial Cell Survival and Interleukin 8 Expression.Reproductive sciences (Thousand Oaks, Calif.) · 2018Article
- Future Directions in Endometriosis Research and Therapeutics.Current women's health reviews · 2018Article
- Recent advances in the understanding of endometriosis: the role of inflammatory mediators in disease pathogenesis and treatment.F1000Research · 2016Review
- The expression of microRNA-451 in human endometriotic lesions is inversely related to that of macrophage migration inhibitory factor (MIF) and regulates MIF expression and modulation of epithelial cell survival.Human reproduction (Oxford, England) · 2015Article
- Article
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 at 2 institutions in 1 country.
Funding
Abstract
Endometriosis is a debilitating disease common in women of reproductive age characterized by pain and infertility. Macrophage migration inhibitory factor (MIF) is a cytokine whose expression is elevated in endometriotic tissue from women with the disease but the functional role of this factor in the pathogenesis of the disease is uncertain. To examine the role of MIF in the pathogenesis of endometriosis, we induced experimental disease in mice and examined the ability of the MIF antagonist, ISO-1, to reduce endometriotic implant size. Administration of ISO-1 resulted in a significant reduction in implant size and vascularity (as assessed by Flk1 mRNA expression) which was not associated with an alteration in the reproductive cycle. These data suggest that inhibition of MIF activity is associated with a significant reduction in endometriotic implant size and leads us to speculate that a similar approach of targeting MIF may prove useful in treating endometriosis in humans.
Indexed as
Identifiers
24790725PMC4002052W2189649558What OpenQuestion holds
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.