ArticleJournal of Crohn's & colitis2023
NOD2 in Crohn's Disease-Unfinished Business.
Article in Journal of Crohn's & colitis, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers, 1 of them a synthesis that pooled it.
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
40 citing papers in PubMed, 1 synthesis or guideline pooled it, 46 citations in OpenAlex.
- Genomic loci and molecular genetic mechanisms for hidradenitis suppurativa.The British journal of dermatology · 2025Pooled it
- Multi-omics characterization of Yao syndrome identifies three pathophysiological axes and disease-specific divergence from Blau syndrome.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Article
- Review
- Translating IBD Genomics into Clinical Practice.Digestive diseases and sciences · 2026Review
- ST8Sia6-dependent glycosylation restrains gut inflammation and pathogenic TCell reports · 2026Article
- An HHEX/IKKα positive feedback loop promotes intestinal inflammation.The Journal of clinical investigation · 2026Article
- Leveraging cell-type specificity and similarity improves single-cell eQTL fine-mapping.Nature communications · 2026Article
- Metabolic orchestration of NOD1 signaling by AMPK-mediated phosphorylation of ZDHHC5.iScience · 2026Article
- eQTL in diseased colon tissue identifies potential target genes associated with IBD.Nature communications · 2026Article
- Inflammatory signaling differentially changes chromatin accessibility and gene expression of the PD- associated kinase LRRK2 between human and mice.bioRxiv : the preprint server for biology · 2026Article
- Mitophagy in inflammatory bowel disease: regulatory mechanisms and therapeutic potential.Frontiers in cell and developmental biology · 2026Review
- AKT-mediated phosphorylation of ZDHHC5 promotes NOD1 palmitoylation and innate immune signaling.Frontiers in immunology · 2026Article
- Gut microbiota dysbiosis and immune responses: insights from IgA nephropathy and inflammatory bowel disease.Frontiers in immunology · 2026Review
- Immunological analysis of Blau syndrome, a unique autoinflammatory state.Frontiers in immunology · 2026Review
- Chemical Profile and In Vitro Protective Effects ofPlants (Basel, Switzerland) · 2025Article
- Rare and common variants in ERAP1 and ERAP2 selected for in response to Yersinia pestis infection contribute to autoimmune disease including inflammatory bowel disease.Mammalian genome : official journal of the International Mammalian Genome Society · 2025Article
- Resolving the field: a role for Nod2 in T cells.Journal of immunology (Baltimore, Md. : 1950) · 2025Review
- Beyond inflammation: what drives the self-perpetuating cycle of fibrosis in IBD?Annals of medicine · 2025Review
- Review
- Combination of mechanical debridement and interleukin 12 or interleukin 23 therapy for refractory facial pyoderma gangrenosum with NOD2 mutation.JAAD case reports · 2025Article
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
Studies of Crohn's disease have consistently implicated NOD2 as the most important gene in disease pathogenesis since first being identified in 2001. Thereafter, genome-wide association, next-generation sequencing and functional analyses have all confirmed a key role for NOD2, but despite this, NOD2 also has significant unresolved complexity. More recent studies have reinvigorated an early hypothesis that NOD2 may be a single-gene cause of disease, and the distinct ileal stricturing phenotype seen with NOD2-related disease presents an opportunity for personalized diagnosis, disease prediction and targeted therapy. The genomics of NOD2 has much that remains unknown, including the role of rare variation, phasing of variants across the haplotype block and the role of variation in the NOD2-regulatory regions. Here, we discuss the evidence and the unmet needs of NOD2 research, based on recently published evidence, and suggest methods that may meet these requirements.
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.