ArticleNature communications2018
NF-κB inducing kinase is a therapeutic target for systemic lupus erythematosus.
Article in Nature communications, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers, 1 of them a synthesis that pooled it.
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.
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Who cites it
58 citing papers in PubMed, 1 synthesis or guideline pooled it, 125 citations in OpenAlex.
- Systemic Lupus Erythematosus and DNA Degradation and Elimination Defects.Frontiers in immunology · 2019Pooled it
- Genomic and transcriptomic correlates of Richter transformation in chronic lymphocytic leukemia.Blood · 2021Trial
- Stress-Dependent NF-κB Signaling in Acute Kidney Injury: Linking Inflammation, Autophagy, and Apoptosis.International journal of molecular sciences · 2026Review
- Noncanonical NF-κB pathway driven inflammation across multiple cellular compartments identifies NIK as a therapeutic target for inflammatory bowel disease.Frontiers in immunology · 2026Article
- Ferroptosis in Autoimmune Diseases: Research Advances and Therapeutic Strategies.International journal of molecular sciences · 2025Review
- NF-κB in inflammation and cancer.Cellular & molecular immunology · 2025Review
- Co-Occurrence of Endometriosis with Systemic Lupus Erythematosus: Genetic Aspects.International journal of molecular sciences · 2025Review
- Targeting NF-kappaB-inducing kinase shapes B-cell homeostasis in myasthenia gravis.Journal of neuroinflammation · 2025Article
- IFNγ-mediated suppression of alternative NF-κB in tumor-resident myeloid cells promotes selective recruitment of cytotoxic but not regulatory T cells.Frontiers in immunology · 2025Article
- The path less traveled: the non-canonical NF-κB pathway in systemic lupus erythematosus.Frontiers in immunology · 2025Review
- Immune metabolic restoration in systemic lupus erythematosus: the impact of gut microbiota, probiotics, and nutritional synergy.Frontiers in immunology · 2025Review
- NIK Is a Mediator of Inflammation and Intimal Hyperplasia in Endothelial Denudation-Induced Vascular Injury.International journal of molecular sciences · 2024Article
- The TNFSF12/TWEAK Modulates Colonic Inflammatory Fibroblast Differentiation and Promotes Fibroblast-Monocyte Interactions.Journal of immunology (Baltimore, Md. : 1950) · 2024Article
- TRAF3 loss-of-function reveals the noncanonical NF-κB pathway as a therapeutic target in diffuse large B cell lymphoma.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- NF-κB in biology and targeted therapy: new insights and translational implications.Signal transduction and targeted therapy · 2024Review
- Transcription Factors in the Pathogenesis of Lupus Nephritis and Their Targeted Therapy.International journal of molecular sciences · 2024Review
- Inhibition of STAT3 alleviates LPS-induced apoptosis and inflammation in renal tubular epithelial cells by transcriptionally down-regulating TASL.European journal of medical research · 2024Article
- Mendelian randomization analysis of causal and druggable circulating inflammatory proteins in schizophrenia.Frontiers in psychiatry · 2024Article
- Development of Allosteric NIK Ligands from Fragment-Based NMR Screening.ACS medicinal chemistry letters · 2023Article
- Accelerating Alchemical Free Energy Prediction Using a Multistate Method: Application to Multiple Kinases.Journal of chemical information and modeling · 2023Article
Corrections and comments
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Authors and funding
35 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
NF-κB-inducing kinase (NIK) mediates non-canonical NF-κB signaling downstream of multiple TNF family members, including BAFF, TWEAK, CD40, and OX40, which are implicated in the pathogenesis of systemic lupus erythematosus (SLE). Here, we show that experimental lupus in NZB/W F1 mice can be treated with a highly selective and potent NIK small molecule inhibitor. Both in vitro as well as in vivo, NIK inhibition recapitulates the pharmacological effects of BAFF blockade, which is clinically efficacious in SLE. Furthermore, NIK inhibition also affects T cell parameters in the spleen and proinflammatory gene expression in the kidney, which may be attributable to inhibition of OX40 and TWEAK signaling, respectively. As a consequence, NIK inhibition results in improved survival, reduced renal pathology, and lower proteinuria scores. Collectively, our data suggest that NIK inhibition is a potential therapeutic approach for SLE.
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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.