ArticleFrontiers in immunology2020
Glucose Induces IL-1α-Dependent Inflammation and Extracellular Matrix Proteins Expression and Deposition in Renal Tubular Epithelial Cells in Diabetic Kidney Disease.
Article in Frontiers in immunology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers, 1 of them a synthesis that pooled it.
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Who cites it
34 citing papers in PubMed, 1 synthesis or guideline pooled it, 46 citations in OpenAlex.
- Pharmacological Nephroprotection in Chronic Kidney Disease Patients with Type 2 Diabetes Mellitus-Clinical Practice Position Statement of the Polish Society of Nephrology.International journal of molecular sciences · 2024Guideline
- Type 2 diabetes mellitus exacerbates vaginal group BmSphere · 2026Article
- Type 2 diabetes mellitus exacerbates vaginal group BbioRxiv : the preprint server for biology · 2026Article
- Innovative Insights into Interleukin-Mediated Macrophage Polarization: Metabolic Reprogramming and Inflammatory Pathway Crosstalk in Chronic Kidney Disease and Therapeutic Implications-A Narrative Review.International journal of general medicine · 2026Review
- Icariside II inhibits ferroptosis and improves high-glucose-induced podocytes injury by downregulating DNMT1.In vitro cellular & developmental biology. Animal · 2026Article
- Hyperglycaemia-induced molecular reprogramming of proximal tubular epithelial cells and its contribution to diabetic kidney disease progression-a narrative review.Frontiers in cell and developmental biology · 2026Review
- IL‑1 receptor antagonism attenuates renal fibrosis via RNF182‑driven MFN2 destabilization and mitochondrial dysfunction.Cell death discovery · 2025Article
- Caffeic acid phenethyl ester protects renal tubular epithelial cells against ferroptosis in diabetic kidney disease via restoring PINK1-mediated mitophagy.Molecular medicine (Cambridge, Mass.) · 2025Article
- Increased Mitochondrial Superoxide Level Is Partially Associated With Vemurafenib-Induced Renal Tubular Toxicity.Basic & clinical pharmacology & toxicology · 2025Article
- Targeting senescence to prevent diabetic kidney disease: Exploring molecular mechanisms and potential therapeutic targets for disease management.Diabetic medicine : a journal of the British Diabetic Association · 2025Review
- Targeting interleukin-1 signaling for renoprotection.Frontiers in immunology · 2025Review
- Glucocorticoid does not improve the renal prognosis of patients with diabetic nephropathy combined with acute tubulointerstitial nephritis: a retrospective analysis.Renal failure · 2024Article
- The Interaction and Implication of Stress-Induced Hyperglycemia and Cytokine Release Following Traumatic Injury: A Structured Scoping Review.Diagnostics (Basel, Switzerland) · 2024Article
- Bidirectional two-sample Mendelian randomization analysis unveils causal association between inflammatory cytokines and the risk of diabetic nephropathy.Scientific reports · 2024Article
- The causal effect of inflammatory proteins and immune cell populations on diabetic nephropathy: evidence from Mendelian randomization.International urology and nephrology · 2024Article
- Roles of Mitochondrial Dysfunction in Diabetic Kidney Disease: New Perspectives from Mechanism to Therapy.Biomolecules · 2024Review
- Anti-Inflammatory Action of Resveratrol in the Central Nervous System in Relation to Glucose Concentration-An In Vitro Study on a Blood-Brain Barrier Model.International journal of molecular sciences · 2024Article
- Identification of crosstalk genes relating to ECM-receptor interaction genes in MASH and DN using bioinformatics and machine learning.Journal of cellular and molecular medicine · 2024Article
- Biomarkers of Arginine Methylation in Diabetic Nephropathy: Novel Insights from Bioinformatics Analysis.Diabetes, metabolic syndrome and obesity : targets and therapy · 2024Article
- Pathomechanisms of Diabetic Kidney Disease.Journal of clinical medicine · 2023Review
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Diabetes mellitus is linked with metabolic stress that induces cellular damage and can provoke renal inflammation and fibrotic responses that eventually lead to chronic kidney disease. Because the inflammasome, interleukin 1 (IL-1), IL-1α/IL-β, and IL-1R are central elements of kidney inflammation and pharmacological IL-1R antagonist (IL-1Ra) was shown to prevent or even reverse diabetic nephropathy (DN) in animal models, we explored the intrinsic expression of IL-1 molecules in kidney tissue of DN patients as regulators of renal inflammation. We used biopsies taken from DN patients and controls and show a high level of IL-1α expression in renal tubular epithelial cells, whereas both IL-1 agonistic molecules (i.e., IL-1α and IL-1β) were devoid of the glomeruli. Human proximal tubular kidney HK-2 cells exposed to high glucose (HG) gradually increase the expression of IL-1α but not IL-1β and induce the expression and deposition of extracellular matrix (ECM) proteins. We further demonstrate that
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