ArticleScientific reports2016
Non-canonical NFκB activation promotes chemokine expression in podocytes.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 30 citations in OpenAlex.
- Efficacy of Dapagliflozin and Telmisartan Combination Therapy in Reducing Albuminuria and Inflammatory Markers in Diabetic Nephropathy: A Prospective Observational Study.Current vascular pharmacology · 2025Observational
- How to Inhibit Nuclear Factor-Kappa B Signaling: Lessons from Poxviruses.Pathogens (Basel, Switzerland) · 2022Review
- Cellular crosstalk of glomerular endothelial cells and podocytes in diabetic kidney disease.Journal of cell communication and signaling · 2022Review
- Lymphotoxin: from the physiology to the regeneration of the thymic function.Cell death and differentiation · 2021Review
- Crosstalk between Heart Failure and Cognitive Impairment via hsa-miR-933/RELB/CCL21 Pathway.BioMed research international · 2021Article
- Inflammasome activation in podocytes: a new mechanism of glomerular diseases.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2020Review
- Article
- Review
- TRAIL, OPG, and TWEAK in kidney disease: biomarkers or therapeutic targets?Clinical science (London, England : 1979) · 2019Review
- Activation of fibroblastic reticular cells in kidney lymph node during crescentic glomerulonephritis.Kidney international · 2019Article
- NFκB and Kidney Injury.Frontiers in immunology · 2019Review
- Repetitive ischemic injuries to the kidneys result in lymph node fibrosis and impaired healing.JCI insight · 2018Article
- TWEAK increases CD74 expression and sensitizes to DDT proinflammatory actions in tubular cells.PloS one · 2018Article
- Valproate hampers podocyte acquisition of immune phenotypes via intercepting the GSK3β facilitated NFkB activation.Oncotarget · 2017Article
- The non-canonical NF-κB pathway in immunity and inflammation.Nature reviews. Immunology · 2017Review
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
TNF-like weak inducer of apoptosis (TWEAK) receptor Fn14 is expressed by podocytes and Fn14 deficiency protects from experimental proteinuric kidney disease. However, the downstream effectors of TWEAK/Fn14 in podocytes are poorly characterized. We have explored TWEAK activation of non-canonical NFκB signaling in cultured podocytes. In cultured podocytes, TWEAK increased the expression of the chemokines CCL21, CCL19 and RANTES in a time-dependent manner. The inhibitor of canonical NFκB activation parthenolide inhibited the CCL19 and the early RANTES responses, but not the CCL21 or late RANTES responses. In this regard, TWEAK induced non-canonical NFκB activation in podocytes, characterized by NFκB2/p100 processing to NFκB2/p52 and nuclear migration of RelB/p52. Silencing by a specific siRNA of NIK, the upstream kinase of the non-canonical NFκB pathway, prevented CCL21 upregulation but did not modulate CCL19 or RANTES expression in response to TWEAK, thus establishing CCL21 as a non-canonical NFκB target in podocytes. Increased kidney Fn14 and CCL21 expression was also observed in rat proteinuric kidney disease induced by puromycin, and was localized to podocytes. In conclusion, TWEAK activates the non-canonical NFκB pathway in podocytes, leading to upregulation of CCL21 expression. The non-canonical NFκB pathway should be explored as a potential therapeutic target in proteinuric kidney disease.
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Registered trials
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