ArticleExperimental & molecular medicine2017
Bcl3: a regulator of NF-κB inducible by TWEAK in acute kidney injury with anti-inflammatory and antiapoptotic properties in tubular cells.
Article in Experimental & molecular medicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 54 citations in OpenAlex.
- Genome-wide CRISPR screens identify shared and context-specific regulators of podocyte resistance to oxidative injury.Renal failure · 2026Article
- Failure of early B cell tolerance and possible BCR signaling dysregulation underlie NF155-mediated autoimmune nodopathies.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Unveiling the multifaceted roles of BCL3: biological functions and disease implications.Apoptosis : an international journal on programmed cell death · 2026Review
- Distinct mechanisms of cell in breast cancer and their clinical implication.Cell biology and toxicology · 2025Review
- Irisin-Loaded Cerium-Containing Mesoporous Bioactive Glass for Effective Immunomodulation and Odontogenesis of Dental Pulp Cells.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Targeting Bcl3/NF-κB p50 Pathway for Neuroinflammation Attenuation and RGCs Protection in Retinal Ischemia/Reperfusion Injury.Investigative ophthalmology & visual science · 2025Article
- Antioxidant, Antiinflammatory and Antiapoptotic Effects of Lycopene in Rats With Vancomycin-Induced Nephrotoxicity.Basic & clinical pharmacology & toxicology · 2025Article
- How PPAR-alpha mediated inflammation may affect the pathophysiology of chronic kidney disease.Current research in physiology · 2025Review
- Herb-CMap: a multimodal fusion framework for deciphering the mechanisms of action in traditional Chinese medicine using Suhuang antitussive capsule as a case study.Briefings in bioinformatics · 2024Article
- Shared genetics and causal association between plasma levels of SARS-CoV-2 entry receptor ACE2 and Alzheimer's disease.CNS neuroscience & therapeutics · 2024Article
- Mechanisms of norcantharidin against renal tubulointerstitial fibrosis.Pharmacological reports : PR · 2024Review
- Article
- The TWEAK/Fn14/CD163 axis-implications for metabolic disease.Reviews in endocrine & metabolic disorders · 2022Review
- Molecular Mechanisms of Kidney Injury and Repair.International journal of molecular sciences · 2022Review
- Bcl-3: A Double-Edged Sword in Immune Cells and Inflammation.Frontiers in immunology · 2022Review
- Nutritional immunomodulation of Atlantic salmon response toFrontiers in molecular biosciences · 2022Article
- The hepatic senescence-associated secretory phenotype promotes hepatocarcinogenesis through Bcl3-dependent activation of macrophages.Cell & bioscience · 2021Article
- Protective and Anti-Inflammatory Effects of Protegrin-1 onInternational journal of molecular sciences · 2021Article
- Genetic Susceptibility to Acute Kidney Injury.Journal of clinical medicine · 2021Review
- Toll-Like Receptors in Acute Kidney Injury.International journal of molecular sciences · 2021Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Acute kidney injury (AKI) is characterized by tubular cell death and interstitial inflammation. TWEAK promotes experimental kidney injury and activates the transcription factor NF-κB, a key regulator of genes involved in cell survival and inflammatory response. In search of potential therapeutic targets for AKI, we compared a transcriptomics database of NF-κB-related genes from murine AKI-kidneys with a transcriptomics database of TWEAK-stimulated cultured tubular cells. Four out of twenty-four (17%) genes were significantly upregulated (false discovery rate, FDR<0.05), while nine out of twenty-four (37%) genes were significantly upregulated at FDR <0.1 in both databases. Bcl3 was the top upregulated NF-κB-related gene in experimental AKI and one of the most upregulated genes in TWEAK-stimulated tubular cells. Quantitative reverse transcription PCR (qRT-PCR), western blot and immunohistochemistry confirmed Bcl3 upregulation in both experimental conditions and localized increased Bcl3 expression to tubular cells in AKI. Transcriptomics database analysis revealed increased Bcl3 expression in numerous experimental and human kidney conditions. Furthermore, systemic TWEAK administration increased kidney Bcl3 expression. In cultured tubular cells, targeting Bcl3 by siRNA resulted in the magnification of TWEAK-induced NF-κB transcriptional activity, chemokine upregulation and Klotho downregulation, and in the sensitization to cell death induced by TWEAK/TNFα/interferon-γ. In contrast, Bcl3 overexpression decreased NF-κB transcriptional activity, inflammatory response and cell death while dampening the decrease in Klotho expression. In conclusion, Bcl3 expressed in response to TWEAK stimulation decreases TWEAK-induced inflammatory and lethal responses. Therefore, therapeutic upregulation of Bcl3 activity should be explored in kidney disease because it has advantages over chemical inhibitors of NF-κB that are known to prevent inflammatory responses but can also sensitize the cells to apoptosis.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.