ArticleJournal of diabetes research2016
Potential of IL-33 for Preventing the Kidney Injury via Regulating the Lipid Metabolism in Gout Patients.
Article in Journal of diabetes research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 26 citations in OpenAlex.
- ST2 + T-Regulatory Cells in Renal Inflammation and Fibrosis after Ischemic Kidney Injury.Journal of the American Society of Nephrology : JASN · 2025Article
- Review
- Article
- Regulating Lipid Metabolism in Gout: A New Perspective with Therapeutic Potential.International journal of general medicine · 2024Review
- The relationship between B-cell lymphoma 2, interleukin-1β, interleukin-17, and interleukin-33 and the development of diabetic nephropathy.Molecular biology reports · 2022Article
- Interleukin 33-mediated inhibition of A-type KTheranostics · 2022Article
- Article
- The anti-inflammatory properties of HDLs are impaired in gout.Clinical rheumatology · 2021Article
- Interleukin-33/ Suppression of Tumorigenicity 2 in Renal Fibrosis: Emerging Roles in Prognosis and Treatment.Frontiers in physiology · 2021Review
- IL-33/ST2 induces neutrophil-dependent reactive oxygen species production and mediates gout pain.Theranostics · 2020Article
- IL33/ST2 Axis in Diabetic Kidney Disease: A Literature Review.Medicina (Kaunas, Lithuania) · 2019Review
- IL-33 at the Crossroads of Metabolic Disorders and Immunity.Frontiers in endocrinology · 2019Review
- IL-33 Ameliorates the Development of MSU-Induced Inflammation Through Expanding MDSCs-Like Cells.Frontiers in endocrinology · 2019Article
- Emerging Roles of IL-33/ST2 Axis in Renal Diseases.International journal of molecular sciences · 2017Review
- Article
- Review
Corrections and comments
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Authors and funding
12 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Interleukin-33 (IL-33), the most recently discovered member of the IL-1 superfamily, has been linked to several human pathologies including autoimmune diseases, sepsis, and allergy through its specific IL-1 receptor ST2. However, there is little information regarding the role of IL-33 in gout. In this study, we investigated the potential role of IL-33 in gout patients. The serum level of IL-33 was measured by ELISA, and the clinical and laboratory parameters, serum creatinine, urea, and lipid, were extracted from medical record system. The serum IL-33 expression was predominantly increased in gout patients compared to healthy controls, and the IL-33 levels were higher in patients without kidney injury. Furthermore, IL-33 showed a negative correlation with biomarkers of kidney injury, such as CRE and urea. The lipid metabolism dysfunction, tophi, and hypertension are the common reasons for kidney injury in gout. Interestingly, inverse and positive correlation of IL-33 expression was observed in LDL and HDL, respectively. However, there was no significant alteration in the gout patients with hypertension and tophi. These data suggested that IL-33 might act as a protective role in kidney injury through regulating the lipid metabolism in gout.
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