ArticleClinical immunology (Orlando, Fla.)2012
Inhibition of the TWEAK/Fn14 pathway attenuates renal disease in nephrotoxic serum nephritis.
Article in Clinical immunology (Orlando, Fla.), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers, 1 of them a synthesis that pooled it.
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Who cites it
52 citing papers in PubMed, 1 synthesis or guideline pooled it, 107 citations in OpenAlex.
- Diagnostic value of TWEAK for predicting active lupus nephritis in patients with systemic lupus erythematosus: a systematic review and meta-analysis.Renal failure · 2021Pooled it
- Application of the nephrotoxic serum nephritis model in glomerulonephritis research.Molecular medicine (Cambridge, Mass.) · 2026Review
- Article
- Revised version with tracked changes oral Magnesium reduces levels of pathogenic autoantibodies and skin disease in murine lupus.BMC immunology · 2024Article
- Transcriptome Analysis of BAFF/BAFF-R System in Murine Nephrotoxic Serum Nephritis.International journal of molecular sciences · 2024Article
- Mechanisms of norcantharidin against renal tubulointerstitial fibrosis.Pharmacological reports : PR · 2024Review
- Pathogenic cellular and molecular mediators in lupus nephritis.Nature reviews. Nephrology · 2023Review
- Iguratimod alleviates tubulo-interstitial injury in mice with lupus.Renal failure · 2022Article
- Inhibition of fibroblast growth factor-inducible 14 attenuates experimental tubulointerstitial fibrosis and profibrotic factor expression of proximal tubular epithelial cells.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2021Article
- Anti-TWEAK Antibody Alleviates Renal Interstitial Fibrosis by Increasing PGC-1α Expression in Lupus Nephritis.Journal of inflammation research · 2021Article
- Ovarian cancer cells direct monocyte differentiation through a non-canonical pathway.BMC cancer · 2020Article
- Article
- ALW peptide ameliorates lupus nephritis in MRL/lpr mice.Arthritis research & therapy · 2019Article
- Fn14 Participates in Neuropathic Pain Through NF-κB Pathway in Primary Sensory Neurons.Molecular neurobiology · 2019Article
- Anti-double Stranded DNA Antibodies: Origin, Pathogenicity, and Targeted Therapies.Frontiers in immunology · 2019Review
- Precision medicine in lupus nephritis: can biomarkers get us there?Translational research : the journal of laboratory and clinical medicine · 2018Review
- Fn14 deficiency ameliorates psoriasis-like skin disease in a murine model.Cell death & disease · 2018Article
- Inflammation and renal fibrosis: Recent developments on key signaling molecules as potential therapeutic targets.European journal of pharmacology · 2018Review
- Fn14 Deficiency Ameliorates Anti-dsDNA IgG-Induced Glomerular Damage in SCID Mice.Journal of immunology research · 2018Article
- Topical TWEAK Accelerates Healing of Experimental Burn Wounds in Mice.Frontiers in pharmacology · 2018Article
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9 authors at 4 institutions in 1 country.
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Abstract
Previously it was shown that the TNF superfamily member TWEAK (TNFSF12) acts through its receptor, Fn14, to promote proinflammatory responses in kidney cells, including the production of MCP-1, RANTES, IP-10 and KC. In addition, the TWEAK/Fn14 pathway promotes mesangial cell proliferation, vascular cell activation, and renal cell death. To study the relevance of the TWEAK/Fn14 pathway in the pathogenesis of antibody-induced nephritis using the mouse model of nephrotoxic serum nephritis (NTN), we induced NTN by passive transfer of rabbit anti-glomerular antibodies into Fn14 knockout (KO) and wild type (WT) mice. Severe proteinuria as well as renal histopathology were induced in WT but not in Fn14 KO mice. Similarly, a pharmacologic approach of anti-TWEAK mAb administration into WT mice in the NTN model significantly ameliorated proteinuria and improved kidney histology. Anti-TWEAK treatment did not affect the generation of mouse anti-rabbit antibodies; however, within the kidney there was a significant decrease in glomerular immunoglobulin deposition, as well as macrophage infiltrates and tubulointerstitial fibrosis. The mechanism of action is most likely due to reductions in downstream targets of TWEAK/Fn14 signaling, including reduced renal expression of MCP-1, VCAM-1, IP-10, RANTES as well as Fn14 itself, and other molecular pathways associated with fibrosis in anti-TWEAK treated mice. Thus, TWEAK/Fn14 interactions are instrumental in the pathogenesis of nephritis in the NTN model, apparently mediating a cascade of pathologic events locally in the kidney rather than by impacting the systemic immune response. Disrupting TWEAK/Fn14 interactions may be an innovative kidney-protective approach for the treatment of lupus nephritis and other antibody-induced renal diseases.
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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.