ArticleMedComm2024
Partial reduction of interleukin-33 signaling improves senescence and renal injury in diabetic nephropathy.
Article in MedComm, 2024. 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.
- Exploratory Effects of a Novel Nutraceutical on Senescence-Related Protein Biomarkers in Healthy Adults: A Pilot Proteomics Study.International journal of molecular sciences · 2026Trial
- Silencing of USP22 promotes FGF11 degradation to attenuates renal fibrosis in diabetic kidney disease.Renal failure · 2026Article
- Trophoblast aging driven by IL33 deficiency elevates recurrent pregnancy loss risk through SNAP29 lactylation-mediated autophagy impairment.Autophagy · 2026Article
- Advanced drug delivery platforms targeting cellular senescence: A promising strategy for cancer therapy.Acta pharmaceutica Sinica. B · 2026Review
- Mechanisms of hesperetin in alleviating diabetic nephropathy: Network pharmacology, molecular docking, and experimental validation.Journal of diabetes investigation · 2026Article
- Beyond the alarm: unveiling the multifaceted role of IL-33 in kidney disease.Frontiers in immunology · 2026Review
- Cellular senescence of renal tubular epithelial cells in diabetic kidney disease: emerging mechanisms and targeted interventions.Frontiers in cell and developmental biology · 2026Review
- Senescence‑associated IL‑33 secretion undermines sorafenib efficacy in hepatocellular carcinoma via immune evasion.Oncology reports · 2025Article
- New Frontiers in the Production of Functional Recombinant Proteins.Bioengineering (Basel, Switzerland) · 2025Article
- The Role of Renal Cell Senescence in Diabetic Kidney Disease: Mechanisms and Therapeutic Advances.Diabetes, metabolic syndrome and obesity : targets and therapy · 2025Review
- Shenyuan granules improve cellular senescence through Klotho-mediated p16/p21 signaling pathway in diabetic kidney disease.Frontiers in medicine · 2025Article
- Research progress on damage-associated molecular patterns in acute kidney injury.Frontiers in immunology · 2025Review
- Partial reduction of interleukin-33 signaling improves senescence and renal injury in diabetic nephropathy.MedComm · 2024Article
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Authors and funding
16 authors.
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Abstract
Diabetic nephropathy (DN) is a frequent and costly complication of diabetes with limited understandings of mechanisms and therapies. Emerging evidence points to the important roles of interleukin-33 (IL-33) in acute kidney injury, yet its contribution to DN is still unclear. We here found a ubiquitous increase of IL-33 and its receptor (ST2) in murine models and patients with DN. Surprisingly, both IL-33 and ST2 knockdown aggravated renal lesions in DN, while overexpression of IL-33 also exacerbated the condition. Further population-based analyses revealed a positive correlation of IL-33 expression with renal dysfunction in DN patients. Individuals with high IL-33 expression-related polygenic risk score had a higher DN risk. These findings confirmed the harmful effects of IL-33 on DN. Conversely, endogenous and exogenous partial reduction of IL-33 signaling conferred renoprotective effects in vivo and in vitro. Mechanistically, IL-33 induced senescence by regulating cell cycle factors in HK-2 cells, and accordingly senescence led to renal cell damage through the secretion of senescence-related secretory phenotype (SASP) including IL-33 and prostaglandins. Together, elevated IL-33 accelerates cellular senescence to drive DN possibly by SASP production, while a partial blockage improves renal injury and senescence. Our findings pinpoint a possible and new avenue for DN interventions.
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