ReviewInflammatory bowel diseases2016
Emerging Roles for Noncanonical NF-κB Signaling in the Modulation of Inflammatory Bowel Disease Pathobiology.
Review in Inflammatory bowel diseases, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 84 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
84 citing papers in PubMed, 162 citations in OpenAlex.
- Regulation of Inducible Nitric Oxide Synthase (NOS2) Expression in Healthy and Inflamed Bowel: A Narrative Review.International journal of molecular sciences · 2026Review
- Cyanidin-3-O-glucoside Alleviates Inflammatory Bowel Disease by Targeting the NF-κB Pathway and is Associated With Alterations in 1-DNJ.Molecular nutrition & food research · 2026Article
- Efficacy of Probiotics and Postbiotics in Treating Dengue Fever - A Potential Strategy to Reduce Antibody-dependent Enhancement.Probiotics and antimicrobial proteins · 2026Review
- Coffea arabica pulp aqueous extract exhibits the anti-colitogenic effect in mice: preventive efficacy and possible mechanisms of action.Biological research · 2026Article
- UHRF1 deficiency exacerbates intestinal inflammation by epigenetic modulation of NPY1R gene methylation.JCI insight · 2026Article
- Research progress on TWEAK/Fn14 signaling in chronic wound healing.Frontiers in surgery · 2026Review
- Regulation of hydrogen and oxidative stress in treating intestinal mucosa from ulcerative colitis.International journal of pharmaceutics: X · 2025Article
- Network pharmacology and molecular docking reveal multi-target mechanisms of Butea monosperma stem bark extract in ulcerative colitis.Scientific reports · 2025Article
- Lactucopicrin: A Sesquiterpene Lactone with Anti-Inflammatory Activity Modulates the Crosstalk between NF-kB and AHR Pathways.Journal of medicinal chemistry · 2025Article
- The Role of Reactive Oxygen Species (ROS) in Periodontitis: A Potential Therapeutic Target.Immunity, inflammation and disease · 2025Review
- Review
- Unraveling the Complexities of Myeloid-Derived Suppressor Cells in Inflammatory Bowel Disease.International journal of molecular sciences · 2025Review
- Article
- Cheese starter cultures attenuate inflammation in the in vitro Caco-2 model.AIMS microbiology · 2025Article
- Perivascular Adipose Tissue Becomes Pro-Contractile and Remodels in an IL10International journal of molecular sciences · 2024Article
- Microbiome- and Host Inflammasome-Targeting Inhibitor Nanoligomers Are Therapeutic in the Murine Colitis Model.ACS pharmacology & translational science · 2024Article
- Anti-Inflammatory Effect of Korean Soybean Sauce (Ganjang) on Mice with Induced Colitis.Journal of microbiology and biotechnology · 2024Article
- Review
- The TNFSF12/TWEAK Modulates Colonic Inflammatory Fibroblast Differentiation and Promotes Fibroblast-Monocyte Interactions.Journal of immunology (Baltimore, Md. : 1950) · 2024Article
- Asiatic acid rescues intestinal tissue by suppressing molecular, biochemical, and histopathological changes associated with the development of ulcerative colitis.Bioscience reports · 2024Article
24 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Crohn's disease and ulcerative colitis are common and debilitating manifestations of inflammatory bowel disease (IBD). IBD is characterized by a radical imbalance in the activation of proinflammatory and anti-inflammatory signaling pathways in the gut. These pathways are controlled by NF-κB, which is a master regulator of gene transcription. In IBD patients, NF-κB signaling is often dysregulated resulting in overzealous inflammation. NF-κB activation occurs through 2 distinct pathways, defined as either canonical or noncanonical. Canonical NF-κB pathway activation is well studied in IBD and is associated with the rapid, acute production of diverse proinflammatory mediators, such as COX-2, IL-1β, and IL-6. In contrast to the canonical pathway, the noncanonical or "alternative" NF-κB signaling cascade is tightly regulated and is responsible for the production of highly specific chemokines that tend to be associated with less acute, chronic inflammation. There is a relative paucity of literature regarding all aspects of noncanonical NF-ĸB signaling. However, it is clear that this alternative signaling pathway plays a considerable role in maintaining immune system homeostasis and likely contributes significantly to the chronic inflammation underlying IBD. Noncanonical NF-κB signaling may represent a promising new direction in the search for therapeutic targets and biomarkers associated with IBD. However, significant mechanistic insight is still required to translate the current basic science findings into effective therapeutic strategies.
Indexed as
Identifiers
What OpenQuestion holds
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.