ReviewInflammatory bowel diseases2014
Emerging significance of NLRs in inflammatory bowel disease.
Review in Inflammatory bowel diseases, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 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
37 citing papers in PubMed, 77 citations in OpenAlex.
- The Safety, Tolerability, Pharmacokinetics, and Clinical Efficacy of the NLRX1 agonist NX-13 in Active Ulcerative Colitis: Results of a Phase 1b Study.Journal of Crohn's & colitis · 2024Trial
- Regulation of Inducible Nitric Oxide Synthase (NOS2) Expression in Healthy and Inflamed Bowel: A Narrative Review.International journal of molecular sciences · 2026Review
- Clinical and genomic features of Iranian patients with very early onset IBD.Pediatric research · 2026Article
- Aimed at Subtype Discrimination but Yielding a Shared Marker: Integrative Analysis of Blood Transcriptomes Reveals UpregulatedClinical and experimental gastroenterology · 2026Article
- Innate Immunity Never "NODs" Off: NLRs Regulate the Host Anti-Viral Immune Response.Immunological reviews · 2025Review
- Molecular Foundations of Inflammatory Diseases: Insights into Inflammation and Inflammasomes.Current issues in molecular biology · 2024Review
- The evolution of NLRC3 subfamily genes in Sebastidae teleost fishes.BMC genomics · 2023Article
- Teleost NOD-like receptors and their downstream signaling pathways: A brief review.Fish and shellfish immunology reports · 2022Review
- The role of NLRP3 inflammasome in colorectal cancer: potential therapeutic target.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2022Review
- Eletrophilic Chemistry of Tranilast Is Involved in Its Anti-Colitic Activity via Nrf2-HO-1 Pathway Activation.Pharmaceuticals (Basel, Switzerland) · 2021Article
- Nod-like Receptors: Critical Intracellular Sensors for Host Protection and Cell Death in Microbial and Parasitic Infections.International journal of molecular sciences · 2021Review
- The Role of Melatonin on NLRP3 Inflammasome Activation in Diseases.Antioxidants (Basel, Switzerland) · 2021Review
- NLRP7 deubiquitination by USP10 promotes tumor progression and tumor-associated macrophage polarization in colorectal cancer.Journal of experimental & clinical cancer research : CR · 2021Article
- Crosstalk Between Intestinal Serotonergic System and Pattern Recognition Receptors on the Microbiota-Gut-Brain Axis.Frontiers in endocrinology · 2021Review
- DNA hypo-methylation facilitates anti-inflammatory responses in severe ulcerative colitis.PloS one · 2021Article
- Ulcerative Colitis-associatedGut microbes · 2020Article
- Telomere dysfunction activates YAP1 to drive tissue inflammation.Nature communications · 2020Article
- CD147 Aggravated Inflammatory Bowel Disease by Triggering NF-BioMed research international · 2020Article
- NEK7 interacts with NLRP3 to modulate the pyroptosis in inflammatory bowel disease via NF-κB signaling.Cell death & disease · 2019Article
- Characterization of genetic subclonal evolution in pancreatic cancer mouse models.Nature communications · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
Pattern recognition receptors are essential mediators of host defense and inflammation in the gastrointestinal system. Recent data have revealed that toll-like receptors and nucleotide-binding domain and leucine-rich repeat-containing proteins (NLRs) function to maintain homeostasis between the host microbiome and mucosal immunity. The NLR proteins are a diverse class of cytoplasmic pattern recognition receptors. In humans, only about half of the identified NLRs have been adequately characterized. The majority of well-characterized NLRs participate in the formation of a multiprotein complex, termed the inflammasome, which is responsible for the maturation of interleukin-1β and interleukin-18. However, recent observations have also uncovered the presence of a novel subgroup of NLRs that function as positive or negative regulators of inflammation through modulating critical signaling pathways, including NF-κB. Dysregulation of specific NLRs from both proinflammatory and inhibitory subgroups have been associated with the development of inflammatory bowel disease (IBD) in genetically susceptible human populations. Our own preliminary retrospective data mining efforts have identified a diverse range of NLRs that are significantly altered at the messenger RNA level in colons from patients with IBD. Likewise, studies using genetically modified mouse strains have revealed that multiple NLR family members have the potential to dramatically modulate the immune response during IBD. Targeting NLR signaling represents a promising and novel therapeutic strategy. However, significant effort is necessary to translate the current understanding of NLR biology into effective therapies.
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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.