ArticleJournal of the American Society of Nephrology : JASN2011
IL-33 exacerbates acute kidney injury.
Article in Journal of the American Society of Nephrology : JASN, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 91 papers.
What it found
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Who cites it
91 citing papers in PubMed, 154 citations in OpenAlex.
- The endothelium response to kidney injury.Nature reviews. Nephrology · 2026Review
- Immunological mechanisms and novel therapeutic strategies for sepsis‑associated acute kidney injury (Review).International journal of molecular medicine · 2026Review
- Role of Serum IL-33 inToxins · 2026Article
- Beyond the alarm: unveiling the multifaceted role of IL-33 in kidney disease.Frontiers in immunology · 2026Review
- ILC imbalance - a new piece in the gut-kidney axis puzzle.Frontiers in immunology · 2026Review
- Immunomodulatory Functions of Intercalated Cells in Kidney Autoimmunity.bioRxiv : the preprint server for biology · 2025Article
- Engineered Neuromedin U Promotes Type 2 Innate Immunity and Renoprotection in Acute Kidney Injury.Journal of the American Society of Nephrology : JASN · 2025Article
- Innate Lymphoid Cells Are the Rheostat of Immune Response in the Kidney.Journal of cellular and molecular medicine · 2025Review
- Innate immune cells in acute and chronic kidney disease.Nature reviews. Nephrology · 2025Review
- Biomarkers as Beacons: Illuminating Sepsis-Associated Hepato-Renal Injury.International journal of molecular sciences · 2025Review
- Review
- Establishment and validation of the prediction model based on lymphocyte subsets for acute kidney injury in sepsis patients.Frontiers in immunology · 2025Article
- Mechanisms Underlying the Impact of Interleukin Family on Acute Kidney Injury: Pathogenesis, Progression, and Therapy.Research (Washington, D.C.) · 2025Review
- Dual Time-Dependent Effects of Interleukin-33 Administration on the Kidney Postmyocardial Infarction.Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research · 2024Article
- Partial reduction of interleukin-33 signaling improves senescence and renal injury in diabetic nephropathy.MedComm · 2024Article
- Combined Plasma Olink Proteomics and Transcriptomics Identifies CXCL1 and TNFRSF12A as Potential Predictive and Diagnostic Inflammatory Markers for Acute Kidney Injury.Inflammation · 2024Article
- Inhibition of Interleukin-33 to Reduce Glomerular Endothelial Inflammation in Diabetic Kidney Disease.Kidney international reports · 2024Article
- Unraveling Chronic Cardiovascular and Kidney Disorder through the Butterfly Effect.Diagnostics (Basel, Switzerland) · 2024Review
- A Deep View of the Biological Property of Interleukin-33 and Its Dysfunction in the Gut.International journal of molecular sciences · 2023Review
- IL-33 induces histidine decarboxylase, especially in c-kitInflammation research : official journal of the European Histamine Research Society ... [et al.] · 2023Article
31 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
13 authors at 3 institutions in 2 countries.
Funding
Abstract
Inflammation contributes to the pathogenesis of acute kidney injury (AKI). IL-33 is a proinflammatory cytokine, but its role in AKI is unknown. Here we observed increased protein expression of full-length IL-33 in the kidney following induction of AKI with cisplatin. To determine whether IL-33 promotes injury, we administered soluble ST2 (sST2), a fusion protein that neutralizes IL-33 activity by acting as a decoy receptor. Compared with cisplatin-induced AKI in untreated mice, mice treated with sST2 had fewer CD4 T cells infiltrate the kidney, lower serum creatinine, and reduced acute tubular necrosis (ATN) and apoptosis. In contrast, administration of recombinant IL-33 (rIL-33) exacerbated cisplatin-induced AKI, measured by an increase in CD4 T cell infiltration, serum creatinine, ATN, and apoptosis; this did not occur in CD4-deficient mice, suggesting that CD4 T cells mediate the injurious effect of IL-33. Wildtype mice that received cisplatin and rIL-33 also had higher levels of the proinflammatory chemokine CXCL1, which CD T cells produce, in the kidney compared with CD4-deficient mice. Mice deficient in the CXCL1 receptor also had lower serum creatinine, ATN, and apoptosis than wildtype mice following cisplatin-induced AKI. Taken together, IL-33 promotes AKI through CD4 T cell-mediated production of CXCL1. These data suggest that inhibiting IL-33 or CXCL1 may have therapeutic potential in AKI.
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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.