ArticleFrontiers in physiology2020
NF-κB System Is Chronically Activated and Promotes Glomerular Injury in Experimental Type 1 Diabetic Kidney Disease.
Article in Frontiers in physiology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers, 2 of them syntheses that pooled it.
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The trial behind it
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Who cites it
32 citing papers in PubMed, 2 syntheses or guidelines pooled it, 57 citations in OpenAlex.
- Lipid Peroxidation in Diabetic Kidney Disease: Mechanism and Natural Solution.International journal of molecular sciences · 2025Pooled it
- Efficacy and Safety of Agomelatine in Depressed Patients with Diabetes: A Systematic Review and Meta-Analysis.International journal of molecular sciences · 2024Pooled it
- Trial
- Article
- Erythropoietin alleviate obstructive renal fibrosis by regulating immunity and inflammation through miR-21-5p/SPRY1/ERK1/2/NF-κB pathway inhibition.Frontiers in molecular biosciences · 2026Article
- Whole Exome Sequencing in 26 Saudi Patients Expands the Mutational and Clinical Spectrum of Diabetic Nephropathy.Medicina (Kaunas, Lithuania) · 2025Article
- REDD1 expression in podocytes facilitates renal inflammation and pyroptosis in streptozotocin-induced diabetic nephropathy.Cell death & disease · 2025Article
- Mesenchymal stem cells suppress kidney injury molecule-1 associated with inhibition of renal PKC/NF-Kβ/STAT3 fibrotic signaling pathway in rats with diabetic nephropathy.Archives of medical science : AMS · 2025Article
- Pathophysiology and emerging biomarkers of cardiovascular-renal-hepato-metabolic syndrome.Frontiers in cardiovascular medicine · 2025Review
- A human stem cell-derived model reveals pathologic extracellular matrix remodeling in diabetic podocyte injury.Matrix biology plus · 2024Article
- Cinnamaldehyde ameliorates diabetes-induced biochemical impairments and AGEs macromolecules in a pre-clinical model of diabetic nephropathy.BMC pharmacology & toxicology · 2024Article
- Molecular Therapeutics for Diabetic Kidney Disease: An Update.International journal of molecular sciences · 2024Review
- Krüppel-like factor 2 is an endoprotective transcription factor in diabetic kidney disease.American journal of physiology. Cell physiology · 2024Review
- Diabetes and Renal Complications: An Overview on Pathophysiology, Biomarkers and Therapeutic Interventions.Biomedicines · 2024Review
- Oxidative Stress: A Culprit in the Progression of Diabetic Kidney Disease.Antioxidants (Basel, Switzerland) · 2024Review
- Phloretamide Protects against Diabetic Kidney Damage and Dysfunction in Diabetic Rats by Attenuating Hyperglycemia and Hyperlipidemia, Suppressing NF-κβ, and Upregulating Nrf2.Pharmaceutics · 2024Article
- PGC1-α in diabetic kidney disease: unraveling renoprotection and molecular mechanisms.Molecular biology reports · 2024Review
- The impact of hypoxia-inducible factors in the pathogenesis of kidney diseases: a link through cell metabolism.Kidney research and clinical practice · 2023Article
- Danzhi Jiangtang capsule reduces renal injury in rats with diabetes induced by high fat diet and streptozotocin downregulating toll-like receptor 4-nuclear factor-κB pathway and apoptosis.Journal of traditional Chinese medicine = Chung i tsa chih ying wen pan · 2023Article
- Endoplasmic Reticulum Stress in Renal Cell Carcinoma.International journal of molecular sciences · 2023Review
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
High glucose concentration can activate TLR4 and NF-κB, triggering the production of proinflammatory mediators. We investigated whether the NF-κB pathway is involved in the pathogenesis and progression of experimental diabetic kidney disease (DKD) in a model of long-term type 1 diabetes mellitus (DM). Adult male Munich-Wistar rats underwent DM by a single streptozotocin injection, and were kept moderately hyperglycemic by daily insulin injections. After 12 months, two subgroups - progressors and non-progressors - could be formed based on the degree of glomerulosclerosis. Only progressors exhibited renal TLR4, NF-κB and IL-6 activation. This scenario was already present in rats with short-term DM (2 months), at a time when no overt glomerulosclerosis can be detected. Chronic treatment with the NF-κB inhibitor, pyrrolidine dithiocarbamate (PDTC), prevented activation of renal TLR4, NF-κB or IL-6, without interfering with blood glucose. PDTC prevented the development of glomerular injury/inflammation and oxidative stress in DM rats. In addition, the NF-κB p65 component was detected in sclerotic glomeruli and inflamed interstitial areas in biopsy material from patients with type 1 DM. These observations indicate that the renal NF-κB pathway plays a key role in the development and progression of experimental DKD, and can become an important therapeutic target in the quest to prevent the progression of human DKD.
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