ReviewFrontiers in immunology2013
TWEAK/Fn14 and Non-Canonical NF-kappaB Signaling in Kidney Disease.
Review in Frontiers in immunology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT05997641 (A Double-Blind, Randomized, Placebo-Controlled, First-in-Human Study to Evaluate the Safety, Tolerability, and Pharmacokinetics of Orally Administered DF-003 Following Single), which is not on this map. Cited by 32 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
A Double-Blind, Randomized, Placebo-Controlled, First-in-Human Study to Evaluate the Safety, Tolerability, and Pharmacokinetics of Orally Administered DF-003 Following Single (Part 1) and Multiple (Part 2) Ascending Doses in Healthy Subjects
Who cites it
32 citing papers in PubMed, 59 citations in OpenAlex.
- Lactate Metabolism-Immune Regulation-Related Gene Signature in Lower-Grade Gliomas: Prognostic Model Development and Immune Characterization.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- Inflammation in cardiovascular-kidney-metabolic syndrome: key roles and underlying mechanisms-a comprehensive review.Molecular and cellular biochemistry · 2025Review
- Multiomic analysis of human kidney disease identifies a tractable inflammatory and pro-fibrotic tubular cell phenotype.Nature communications · 2025Article
- Article
- Identification and study of new NF-κB-inducing kinase ligands derived from the imidazolone scaffold.Archiv der Pharmazie · 2025Article
- Article
- Unraveling the proteomic landscape of fibrosis in lupus nephritis through CI-based analysis.Clinical rheumatology · 2024Article
- NIK Is a Mediator of Inflammation and Intimal Hyperplasia in Endothelial Denudation-Induced Vascular Injury.International journal of molecular sciences · 2024Article
- Combined Plasma Olink Proteomics and Transcriptomics Identifies CXCL1 and TNFRSF12A as Potential Predictive and Diagnostic Inflammatory Markers for Acute Kidney Injury.Inflammation · 2024Article
- Development of a Model of Tubulointerstitial Fibrosis Using Transient Unilateral Renal Ischemia and Delayed Contralateral Nephrectomy in Domesticated Cats.Comparative medicine · 2024Article
- Lysophosphatidic Acid Is a Proinflammatory Stimulus of Renal Tubular Epithelial Cells.International journal of molecular sciences · 2022Article
- Crosstalk between TBK1/IKKε and the type I interferon pathway contributes to tubulointerstitial inflammation and kidney tubular injury.Frontiers in pharmacology · 2022Article
- Serum RelB is correlated with renal fibrosis and predicts chronic kidney disease progression.Clinical and translational medicine · 2021Article
- Review
- Review
- A journey from microenvironment to macroenvironment: the role of metaflammation and epigenetic changes in cardiorenal disease.Clinical kidney journal · 2019Article
- Molecular Mechanisms of Epigallocatechin-3-Gallate for Prevention of Chronic Kidney Disease and Renal Fibrosis: Preclinical Evidence.Current developments in nutrition · 2019Review
- Inflammation and renal fibrosis: Recent developments on key signaling molecules as potential therapeutic targets.European journal of pharmacology · 2018Review
- Article
- Tumor necrosis factor-like weak inducer of apoptosis induces inflammation in Graves' orbital fibroblasts.PloS one · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The incidence of acute kidney injury (AKI) and chronic kidney disease (CKD) is increasing. However, there is no effective therapy for AKI and current approaches only slow down, but do not prevent progression of CKD. TWEAK is a TNF superfamily cytokine. A solid base of preclinical data suggests a role of therapies targeting the TWEAK or its receptor Fn14 in AKI and CKD. In particular TWEAK/Fn14 targeting may preserve renal function and decrease cell death, inflammation, proteinuria, and fibrosis in mouse animal models. Furthermore there is clinical evidence for a role of TWEAK in human kidney injury including increased tissue and/or urinary levels of TWEAK and parenchymal renal cell expression of the receptor Fn14. In this regard, clinical trials of TWEAK targeting are ongoing in lupus nephritis. Nuclear factor-kappa B (NF-κB) activation plays a key role in TWEAK-elicited inflammatory responses. Activation of the non-canonical NF-κB pathway is a critical difference between TWEAK and TNF. TWEAK activation of the non-canonical NF-κB pathways promotes inflammatory responses in tubular cells. However, there is an incomplete understanding of the role of non-canonical NF-κB activation in kidney disease and on its contribution to TWEAK actions in vivo.
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Registered trials
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.