ArticleJournal of the American Society of Nephrology : JASN2016
Tubular Epithelial NF-κB Activity Regulates Ischemic AKI.
Article in Journal of the American Society of Nephrology : JASN, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 112 papers.
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Who cites it
112 citing papers in PubMed, 177 citations in OpenAlex.
- A fasting-mimicking diet in patients with mild-to-moderate Crohn's disease: a randomized controlled trial.Nature medicine · 2026Trial
- Nucleic acid sensing pathways in kidney disease development.Nature reviews. Nephrology · 2026Review
- URB597 attenuates experimental sepsis-associated acute kidney injury with reduced renal inflammation, apoptosis, and TLR4/NF-κB activation.Molecular biology reports · 2026Article
- NAT10-mediated acCellular & molecular biology letters · 2026Article
- NF-κB-driven lymphangiogenesis affects kidney function via a VEGFR-3-mediated pathway.JCI insight · 2026Article
- Cell-cell crosstalk in kidney health and disease.Nature reviews. Nephrology · 2026Review
- Exploring the Therapeutic Role of Pregnane X Receptor Activation in Acute Kidney Injury: Mechanisms and Clinical Implications.Current molecular medicine · 2026Review
- Membranous nephropathy preceding Bing-Neel syndrome: successful treatment with tirabrutinib.Journal of nephrology · 2025Article
- Inhibition of Axl attenuates acute kidney injury by alleviating inflammation via SOCS3 downregulation in tubular epithelial cells.BMC nephrology · 2025Article
- Translocation of gut bacteria promotes tumor-associated mortality by inducing immune-activated renal damage.The EMBO journal · 2025Article
- Nfkb1 Removal from Proximal Tubule Cells Improves Renal Tubular Outcomes Following Ischemia Reperfusion Injury.Kidney360 · 2025Article
- Navigating the Complex Pathogenesis of Acute Kidney Injury: Exploring Macrophage Dynamics, Mitochondrial Dysfunction, and Ferroptosis Pathways.Advances in kidney disease and health · 2025Review
- Tubular CD44 plays a key role in aggravating AKI through NF-κB p65-mediated mitochondrial dysfunction.Cell death & disease · 2025Article
- Gender Differences in Adenine Diet-Induced Kidney Toxicity: The Impact of 17β-Estradiol on Renal Inflammation and Fibrosis.International journal of molecular sciences · 2025Article
- SREBP1c-Mediated Transcriptional Repression of YME1L1 Contributes to Acute Kidney Injury by Inducing Mitochondrial Dysfunction in Tubular Epithelial Cells.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Protective effect of Panax ginseng extract on cisplatin-induced AKI via downregulating cell death associated genes.Scientific reports · 2025Article
- 5-Hydroxytryptamine 1F Receptor Agonist Lasmiditan Differentially Regulates Successful Repair and Failed Repair Genes in a Mouse Model of Acute Kidney Injury.ACS pharmacology & translational science · 2024Article
- [Quercetin ameliorates diabetic kidney injury in rats by inhibiting the HMGB1/RAGE/NF-κB signaling pathway].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2024Article
- A pilot study on the differential urine proteomic profile of subjects with community-acquired acute kidney injury who recover versus those who do not recover completely at 4 months after hospital discharge.Frontiers in medicine · 2024Article
- Epigenetic reprogramming driving successful and failed repair in acute kidney injury.Science advances · 2024Article
52 more citing papers are in PubMed but not listed here.
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Authors and funding
15 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
NF-κB is a key regulator of innate and adaptive immunity and is implicated in the pathogenesis of AKI. The cell type-specific functions of NF-κB in the kidney are unknown; however, the pathway serves distinct functions in immune and tissue parenchymal cells. We analyzed tubular epithelial-specific NF-κB signaling in a mouse model of ischemia-reperfusion injury (IRI)-induced AKI. NF-κB reporter activity and nuclear localization of phosphorylated NF-κB subunit p65 analyses in mice revealed that IRI induced widespread NF-κB activation in renal tubular epithelia and in interstitial cells that peaked 2-3 days after injury. To genetically antagonize tubular epithelial NF-κB activity, we generated mice expressing the human NF-κB super-repressor IκBαΔN in renal proximal, distal, and collecting duct epithelial cells. Compared with control mice, these mice exhibited improved renal function, reduced tubular apoptosis, and attenuated neutrophil and macrophage infiltration after IRI-induced AKI. Furthermore, tubular NF-κB-dependent gene expression profiles revealed temporally distinct functional gene clusters for apoptosis, chemotaxis, and morphogenesis. Primary proximal tubular cells isolated from IκBαΔN-expressing mice and exposed to hypoxia-mimetic agent cobalt chloride exhibited less apoptosis and expressed lower levels of chemokines than cells from control mice did. Our results indicate that postischemic NF-κB activation in renal tubular epithelia aggravates tubular injury and exacerbates a maladaptive inflammatory response.
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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.