ArticleJournal of cellular and molecular medicine2019
Macrophage migration inhibitory factor promotes renal injury induced by ischemic reperfusion.
Article in Journal of cellular and molecular medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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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.
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Who cites it
23 citing papers in PubMed, 39 citations in OpenAlex.
- NAT10-mediated acCellular & molecular biology letters · 2026Article
- Biphasic protective effects of macrophage migration inhibitory factor in ischemia/reperfusion-induced acute kidney injury.Communications biology · 2025Article
- Innate immune cells in acute and chronic kidney disease.Nature reviews. Nephrology · 2025Review
- Kidney immunology from pathophysiology to clinical translation.Nature reviews. Immunology · 2025Review
- Hypothermic machine perfusion prevents hyperacute graft loss in pig-to-primate kidney xenotransplantation after 5-hours of cold Ischemia.Communications medicine · 2025Article
- Calycosin inhibited MIF-mediated inflammatory chemotaxis of macrophages to ameliorate ischemia reperfusion-induced acute kidney injury.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2024Article
- Macrophage-derived macrophage migration inhibitory factor mediates renal injury in anti-glomerular basement membrane glomerulonephritis.Frontiers in immunology · 2024Article
- Dexmedetomidine reduces myocardial ischemia-reperfusion injury in young mice through MIF/AMPK/GLUT4 axis.BMC anesthesiology · 2022Article
- Macrophage Migration Inhibitory Factor (MIF) as a Stress Molecule in Renal Inflammation.International journal of molecular sciences · 2022Review
- Macrophage migration inhibitory factor family proteins are multitasking cytokines in tissue injury.Cellular and molecular life sciences : CMLS · 2022Review
- Macrophage migration inhibitory factor in acute kidneyinjury.Frontiers in physiology · 2022Review
- Article
- Genetic Susceptibility to Acute Kidney Injury.Journal of clinical medicine · 2021Review
- Major signaling pathways and key mediators of macrophages in acute kidney injury (Review).Molecular medicine reports · 2021Review
- Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2): a Systemic Infection.Clinical microbiology reviews · 2021Review
- Changes of Urinary Cytokines in Non-Diabetic Obese Patients After Laparoscopic Sleeve Gastrectomy.International journal of general medicine · 2021Article
- Lung Cancer Cell-Derived Secretome Mediates Paraneoplastic Inflammation and Fibrosis in Kidney in Mice.Cancers · 2020Article
- Neural transcription factor Pou4f1 promotes renal fibrosis via macrophage-myofibroblast transition.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Erythropoietin Ameliorates Ischemia/Reperfusion-Induced Acute Kidney Injury via Inflammasome Suppression in Mice.International journal of molecular sciences · 2020Article
- Phillyrin Relieves Lipopolysaccharide-Induced AKI by Protecting Against Glycocalyx Damage and Inhibiting Inflammatory Responses.Inflammation · 2020Article
Corrections and comments
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Authors and funding
16 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Macrophage migration inhibitory factor (MIF) is pleiotropic cytokine that has multiple effects in many inflammatory and immune diseases. This study reveals a potential role of MIF in acute kidney injury (AKI) in patients and in kidney ischemic reperfusion injury (IRI) mouse model in MIF wild-type (WT) and MIF knockout (KO) mice. Clinically, plasma and urinary MIF levels were largely elevated at the onset of AKI, declined to normal levels when AKI was resolved and correlated tightly with serum creatinine independent of disease causes. Experimentally, MIF levels in plasma and urine were rapidly elevated after IRI-AKI and associated with the elevation of serum creatinine and the severity of tubular necrosis, which were suppressed in MIF KO mice. It was possible that MIF may mediate AKI via CD74/TLR4-NF-κB signalling as mice lacking MIF were protected from AKI by largely suppressing CD74/TLR-4-NF-κB associated renal inflammation, including the expression of MCP-1, TNF-α, IL-1β, IL-6, iNOS, CXCL15(IL-8 in human) and infiltration of macrophages, neutrophil, and T cells. In conclusion, our study suggests that MIF may be pathogenic in AKI and levels of plasma and urinary MIF may correlate with the progression and regression of AKI.
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Registered trials
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