ArticleBMC nephrology2023
IL-33/ST2L signaling alleviates diabetic nephropathy by regulating endoplasmic reticulum stress and apoptosis.
Article in BMC nephrology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 15 citations in OpenAlex.
- The IL-33/ST2 Signaling Axis Alleviates Splenic Injury in Severe Acute Pancreatitis by Inhibiting T-Cell Ferroptosis.Pancreas · 2026Article
- Multiomics Integration Analysis Reveals the Regulatory Mechanisms of Efferocytosis in Diabetic Kidney Disease.Inflammation · 2026Article
- Beyond the alarm: unveiling the multifaceted role of IL-33 in kidney disease.Frontiers in immunology · 2026Review
- Intermodulation of endoplasmic reticulum stress and ferroptosis in diabetic nephropathy: molecular mechanisms and therapeutic potentials.Apoptosis : an international journal on programmed cell death · 2025Review
- Immunomodulatory Functions of Intercalated Cells in Kidney Autoimmunity.bioRxiv : the preprint server for biology · 2025Article
- Novel therapeutic target for diabetic kidney disease through downregulation of miRNA-192-5p and miRNA-21-5p by celastrol: implication of autophagy, oxidative stress, and fibrosis.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- Soluble suppression of tumorigenicity 2 associated with contrast-induced acute kidney injury in patients with STEMI.International urology and nephrology · 2025Observational
- TheInternational journal of molecular sciences · 2024Article
- Partial reduction of interleukin-33 signaling improves senescence and renal injury in diabetic nephropathy.MedComm · 2024Article
- IL-33 Signaling Inhibition Leads to a Preeclampsia-Like Phenotype in Pregnant Rats.American journal of reproductive immunology (New York, N.Y. : 1989) · 2024Article
- Depression of LncRNA DANCR alleviates tubular injury in diabetic nephropathy by regulating KLF5 through sponge miR-214-5p.BMC nephrology · 2024Article
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8 authors at 1 institution in 1 country.
Funding
Abstract
objectiveDiabetic nephropathy (DN) is a serious chronic complication of diabetes mellitus (DM). Endoplasmic reticulum (ER) stress is an important factor in the regulation of pathological processes in DN, and excessive ER stress can lead to apoptosis. Although the IL-33/ST2 axis is known to be involved in diabetic kidney disease or related nephropathy, its role and molecular mechanisms remain poorly understood in terms of DN. The purpose of this study was to investigate the effects of IL-33/ST2 signaling on DN and to characterize the roles that ER stress and apoptosis play in DN.
methodsTo investigate this study, mice were randomly assigned into DN (induced by 0.1% STZ) and Control groups. Biochemical indices (FBG, BUN, UPR, UCE) were measured in serum and urine samples to reflect blood glucose and kidney damage. Quantitative real-time PCR, western blot, and immunofluorescence were used to assess gene and protein expression of the IL-33/ST2 axis and ER stress relative signaling molecule. Apoptosis was analyzed by flow cytometry.
resultsIL-33 levels are significantly increased in the kidneys of patients and mice with DN. Double immunofluorescence staining showed that IL-33 colocalized with CD31-positive endothelial cells. Treatment with IL-33 attenuated kidney injury in Streptozotocin (STZ)-treated mice. In vitro, we showed that IL-33 attenuated ER stress and apoptosis in glomerular endothelial cells. However, sST2 treatment significantly reversed these effects of IL-33.
conclusionTogether, these data suggest that IL-33/ST2 signaling mitigates STZ-induced renal damage, partly at least, by suppressing ER stress and apoptosis. Therefore, IL-33 may be an effective therapeutic target in DN.
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