ArticleJournal of leukocyte biology2015
Macrophage migration inhibitory factor is required for recruitment of scar-associated macrophages during liver fibrosis.
Article in Journal of leukocyte biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 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
35 citing papers in PubMed, 53 citations in OpenAlex.
- Reprogramming macrophages to treat liver diseases.Hepatology (Baltimore, Md.) · 2026Review
- MIF inhibition attenuates proliferative vitreoretinopathy pathogenesis and protects the eye in preclinical model.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2026Article
- Role of Scar-Associated Macrophages in Organ Fibrosis Diseases.Journal of immunology research · 2026Review
- The multifaced role of the macrophage migration inhibitory factor family in organ fibrosis.American journal of physiology. Cell physiology · 2025Review
- HBV sequence integrated to enhancer acting as oncogenic driver epigenetically promotes hepatocellular carcinoma development.Journal of experimental & clinical cancer research : CR · 2025Article
- Macrophage heterogeneity in liver fibrosis.Frontiers in immunology · 2025Review
- An engineered adipose formulation decreases hepatic inflammation and fibrosis in a rodent model of metabolic dysfunction-associated steatotic liver disease.Frontiers in bioengineering and biotechnology · 2025Article
- Comprehensive proteomic characterization of urethral stricture disease in the Chinese population.Frontiers in molecular biosciences · 2024Article
- Sja-Let-7 Attenuates Carbon Tetrachloride-Induced Liver Fibrosis in a Mouse Model via Col1α2.Biology · 2023Article
- Understanding the Potential Role of Nanotechnology in Liver Fibrosis: A Paradigm in Therapeutics.Molecules (Basel, Switzerland) · 2023Review
- Role of the chemokine system in liver fibrosis: a narrative review.Digestive medicine research · 2022Article
- Macrophage migration inhibitory factor family proteins are multitasking cytokines in tissue injury.Cellular and molecular life sciences : CMLS · 2022Review
- MIF promotes cell invasion by the LRP1-uPAR interaction in pancreatic cancer cells.Frontiers in oncology · 2022Article
- Is the Macrophage Phenotype Determinant for Fibrosis Development?Biomedicines · 2021Review
- Review
- Review
- Endothelial p300 Promotes Portal Hypertension and Hepatic Fibrosis Through C-C Motif Chemokine Ligand 2-Mediated Angiocrine Signaling.Hepatology (Baltimore, Md.) · 2021Article
- Macrophages in Chronic Liver Failure: Diversity, Plasticity and Therapeutic Targeting.Frontiers in immunology · 2021Review
- Breast cancer resistance protein (Bcrp/Abcg2) is selectively modulated by lipopolysaccharide (LPS) in the mouse yolk sac.Reproductive toxicology (Elmsford, N.Y.) · 2020Article
- Review
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
Recruitment of peripheral monocytes to the liver is a key contributor to the response to injury. MIF can act as a chemokine and cytokine, regulating innate immune responses in many tissues and cell types. We hypothesized that MIF contributes to the progression of CCl4-induced hepatic fibrosis by regulating recruitment of SAM. SAMs dynamically regulate HSC activation and ECM degradation. To gain insight into the role of MIF in progression of liver fibrosis, we investigated markers of fibrosis and immune responses after chronic CCl4 administration to female C57BL/6 and MIF(-/-) mice. Chronic CCl4 exposure increased activation of HSC in WT mice, indicated by increased expression of αSMA mRNA and protein, as well as mRNA for collagen 1α1; these responses were blunted in female MIF(-/-) mice. Despite lower activation of HSC in MIF(-/-) mice, accumulation of ECM was similar in WT and MIF(-/-)mice, suggesting a decreased rate of ECM degradation. Recruitment of SAMs was lower in MIF(-/-) mice compared with WT mice, both in their initial inflammatory phenotype, as well as in the later phase as proresolution macrophages. The decreased presence of resolution macrophages was associated with lower expression of MMP13 in MIF(-/-) mice. Taken together, these data indicate that MIF-dependent recruitment of SAMs contributes to degradation of ECM via MMP13, highlighting the importance of appropriate recruitment and phenotypic profile of macrophages in the resolution of fibrosis.
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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.