ArticleAmerican journal of physiology. Renal physiology2018
IL-33 deficiency slows cancer growth but does not protect against cisplatin-induced AKI in mice with cancer.
Article in American journal of physiology. Renal physiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 14 citations in OpenAlex.
- Beyond the alarm: unveiling the multifaceted role of IL-33 in kidney disease.Frontiers in immunology · 2026Review
- Bardoxolone methyl improves survival and reduces clinical measures of kidney injury in tumor-bearing mice treated with cisplatin.AAPS open · 2025Article
- Understanding Cisplatin Pharmacokinetics and Toxicodynamics to Predict and Prevent Kidney Injury.The Journal of pharmacology and experimental therapeutics · 2024Review
- Experimental models for preclinical research in kidney disease.Zoological research · 2024Review
- The Role of Vascular-Immune Interactions in Modulating Chemotherapy Induced Neuropathic Pain.Frontiers in pharmacology · 2022Article
- Review
- HIF in Nephrotoxicity during Cisplatin Chemotherapy: Regulation, Function and Therapeutic Potential.Cancers · 2021Review
- The effect of MEK1/2 inhibitors on cisplatin-induced acute kidney injury (AKI) and cancer growth in mice.Cellular signalling · 2020Article
- Emerging Roles of Interleukin-33-responsive Kidney Group 2 Innate Lymphoid Cells in Acute Kidney Injury.International journal of molecular sciences · 2020Review
- Capillary rarefaction is more closely associated with CKD progression after cisplatin, rhabdomyolysis, and ischemia-reperfusion-induced AKI than renal fibrosis.American journal of physiology. Renal physiology · 2019Article
- Recent Advances in Models, Mechanisms, Biomarkers, and Interventions in Cisplatin-Induced Acute Kidney Injury.International journal of molecular sciences · 2019Review
- The Role of IL-33/ST2 Pathway in Tumorigenesis.International journal of molecular sciences · 2018Review
- Endogenous IL-33 Contributes to Kidney Ischemia-Reperfusion Injury as an Alarmin.Journal of the American Society of Nephrology : JASN · 2018Article
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Authors and funding
12 authors at 3 institutions in 2 countries.
Funding
Abstract
The effect of IL-33 deficiency on acute kidney injury (AKI) and cancer growth in a 4-wk model of cisplatin-induced AKI in mice with cancer was determined. Mice were injected subcutaneously with murine lung cancer cells. Ten days later, cisplatin (10 mg·kg-¹·wk-¹) was administered weekly for 4 wk. The increase in kidney IL-33 preceded the AKI and tubular injury, suggesting that IL-33 may play a causative role. However, the increase in serum creatinine, blood urea nitrogen, serum neutrophil gelatinase-associated lipoprotein, acute tubular necrosis, and apoptosis scores in the kidney in cisplatin-induced AKI was the same in wild-type and IL-33-deficient mice. There was an increase in kidney expression of pro-inflammatory cytokines CXCL1 and TNF-α, known mediators of cisplatin-induced AKI, in IL-33-deficient mice. Surprisingly, tumor weight, tumor volume, and tumor growth were significantly decreased in IL-33-deficient mice, and the effect of cisplatin on tumors was enhanced in IL-33-deficient mice. As serum IL-33 was increased in cisplatin-induced AKI in mice, it was determined whether serum IL-33 is an early biomarker of AKI in patients undergoing cardiac surgery. Immediate postoperative serum IL-33 concentrations were higher in matched AKI cases compared with non-AKI controls. In conclusion, even though the cancer grows slower in IL-33-deficient mice, the data that IL-33 deficiency does not protect against AKI in a clinically relevant model suggest that IL-33 inhibition may not be useful to attenuate AKI in patients with cancer. However, serum IL-33 may serve as a biomarker of AKI.
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Registered trials
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