ArticleJournal of the American Society of Nephrology : JASN2010
NFkappaB promotes inflammation, coagulation, and fibrosis in the aging glomerulus.
Article in Journal of the American Society of Nephrology : JASN, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.
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Who cites it
46 citing papers in PubMed, 92 citations in OpenAlex.
- Possible contribution of the STAT3 signaling pathway to disseminated intravascular coagulation (DIC) in mice with cecal ligation and puncture-induced sepsis.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Capilliposide A attenuates diabetic nephropathy via modulation of NF-κB/TLR4 and apoptotic pathways.Scientific reports · 2025Article
- The Dual Role of Cellular Senescence in Macrophages: Unveiling the Hidden Driver of Age-Related Inflammation in Kidney Disease.International journal of biological sciences · 2025Review
- Targeting endothelin signaling in podocyte injury and diabetic nephropathy-diabetic kidney disease.Journal of nephrology · 2025Review
- Endothelial Dysfunction Biomarkers and CKD Incidence in the REGARDS Cohort.Kidney international reports · 2024Article
- Precision nephrology identified tumor necrosis factor activation variability in minimal change disease and focal segmental glomerulosclerosis.Kidney international · 2023Article
- Activation of STAT3 signaling pathway in the kidney of COVID-19 patients.Journal of nephrology · 2022Observational
- The Aging Kidney-As Influenced by Heavy Metal Exposure and Selenium Supplementation.Biomolecules · 2021Review
- Generation of a novel decay accelerating factor (DAF) knock-out rat model using clustered regularly-interspaced short palindromic repeats, (CRISPR)/associated protein 9 (Cas9), genome editing.Transgenic research · 2021Article
- Soluble RARRES1 induces podocyte apoptosis to promote glomerular disease progression.The Journal of clinical investigation · 2020Article
- Downregulated PEG3 ameliorates cardiac fibrosis and myocardial injury in mice with ischemia/reperfusion through the NF-κB signaling pathway.Journal of bioenergetics and biomembranes · 2020Article
- Anti-aging Effects of Calorie Restriction (CR) and CR Mimetics based on the Senoinflammation Concept.Nutrients · 2020Review
- Tyro3 is a podocyte protective factor in glomerular disease.JCI insight · 2018Article
- Article
- Glomerular function in relation to circulating adhesion molecules and inflammation markers in a general population.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2018Article
- A molecular morphometric approach to diabetic kidney disease can link structure to function and outcome.Kidney international · 2018Article
- FSGS as an Adaptive Response to Growth-Induced Podocyte Stress.Journal of the American Society of Nephrology : JASN · 2017Article
- Cellular senescence, senescence-associated secretory phenotype, and chronic kidney disease.Oncotarget · 2017Review
- Inflammation and elevated levels of fibroblast growth factor 23 are independent risk factors for death in chronic kidney disease.Kidney international · 2017Observational
- Mitogen-Activated Protein Kinase 14 Promotes AKI.Journal of the American Society of Nephrology : JASN · 2017Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
Abstract
The peak prevalence of ESRD from glomerulosclerosis occurs at 70 to 79 years. To understand why old glomeruli are prone to failure, we analyzed the Fischer 344 rat model of aging under ad libitum-fed (rapid aging) and calorie-restricted (slowed aging) conditions. All glomerular cells contained genes whose expression changed "linearly" during adult life from 2 to 24 months: mesangial cells (e.g., MMP9), endothelial cells (e.g., ICAM and VCAM), parietal epithelial cells (e.g., ceruloplasmin), and podocytes (e.g., nephrin and prepronociceptin). Patterns of aging glomerular gene expression closely resembled atherosclerosis, including activation of endothelial cells, epithelial cells, and macrophages, as well as proinflammatory pathways related to cell adhesion, chemotaxis, blood coagulation, oxidoreductases, matrix metalloproteinases, and TGF-beta activation. We used a nonbiased data-mining approach to identify NFkappaB as the likely transcriptional regulator of these events. We confirmed NFkappaB activation by two independent methods: translocation of NFkappaB p50 to glomerular nuclei and ChIP assays demonstrating NFkappaB p50 binding to the kappaB motif of target genes in old versus young glomeruli. These data suggest that old glomeruli exhibit NFkappaB-associated up-regulation of a proinflammatory, procoagulable, and profibrotic phenotype compared with young glomeruli; these distinctions could explain their enhanced susceptibility to failure. Furthermore, these results provide a potential mechanistic explanation for the close relationship between ESRD and atherosclerotic organ failure as two parallel arms of age-associated NFkappaB-driven processes.
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Registered trials
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