ReviewGut2011
Crohn's disease: NOD2, autophagy and ER stress converge.
Review in Gut, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 106 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
106 citing papers in PubMed, 1 synthesis or guideline pooled it, 224 citations in OpenAlex.
- Pooled it
- Deciphering the Implications ofPathogens (Basel, Switzerland) · 2026Review
- Canonical pathways and selective mechanisms of autophagy in inflammatory bowel disease.Advanced biotechnology · 2026Review
- Endoplasmic reticulum stress as a mechanistic link between nutrition and inflammatory bowel disease.Frontiers in nutrition · 2026Review
- Intestinal toxicity of functionalized polystyrene nanoplastics in NOD2 models of Crohn's disease susceptibility.Frontiers in toxicology · 2026Article
- Current status and future perspectives of multi-modal bacteria-based cancer therapies.Clinical and translational medicine · 2025Review
- Therapeutic mechanisms of exclusive enteral nutrition in Crohn's disease.Seminars in immunopathology · 2025Review
- Dehydrodiisoeugenol targets NOD2 exerting dual effects against colitis and colorectal cancer: a double-edged sword.Molecular medicine (Cambridge, Mass.) · 2025Article
- MAPK signaling mediated intestinal inflammation induced by endoplasmic reticulum stress and NOD2.Molecular and cellular biochemistry · 2025Article
- Endoplasmic reticulum stress in gut inflammation: Implications for ulcerative colitis and Crohn's disease.World journal of gastroenterology · 2025Review
- ATG16L1 restrains macrophage NLRP3 activation and alveolar epithelial cell injury during septic lung injury.Clinical and translational medicine · 2025Article
- Gut microbiota interplay with autophagy-EMT dynamics in colorectal cancer.Frontiers in cell and developmental biology · 2025Review
- Macrophage LRRK2 hyperactivity impairs autophagy and induces Paneth cell dysfunction.Science immunology · 2024Article
- Deubiquitinase USP14 is upregulated in Crohn's disease and inhibits the NOD2 pathway mediated inflammatory responseEuropean journal of histochemistry : EJH · 2024Article
- Shared Pathophysiology of Inflammatory Bowel Disease and Psoriasis: Unraveling the Connection.Cureus · 2024Review
- Role and molecular mechanism of NOD2 in chronic non-communicable diseases.Journal of molecular medicine (Berlin, Germany) · 2024Review
- Transcriptome-wide association studies associated with Crohn's disease: challenges and perspectives.Cell & bioscience · 2024Review
- Interleukin-22 suppresses major histocompatibility complex II in mucosal epithelial cells.The Journal of experimental medicine · 2023Article
- Lung Involvement in Inflammatory Bowel Diseases: Shared Pathways and Unwanted Connections.Journal of clinical medicine · 2023Review
- Inflammatory Bowel Diseases: An Updated Overview on the Heat Shock Protein Involvement.International journal of molecular sciences · 2023Review
46 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
5 authors at 2 institutions in 2 countries.
Funding
Abstract
Polymorphisms in NOD2, encoding an intracellular pattern recognition receptor, contribute the largest fraction of genetic risk for Crohn's disease among the >40 risk loci identified so far. Autophagy plays a prominent role in the innate immune response towards intracellular bacteria. The discovery of the autophagy genes ATG16L1 and IRGM as risk factors for Crohn's disease turned autophagy into the spotlight in inflammatory bowel disease (IBD). Remarkably, NOD2 has recently been identified as a potent autophagy inducer. A physical interaction of NOD2 and ATG16L1 appears to be required for autophagic clearance of intracellular pathogens. Moreover, Crohn's disease-associated NOD2 and ATG16L1 variants exhibit a defect in the induction of an autophagic response and hence predict autophagy as a key converging mechanism that leads to Crohn's disease. Another pathway that is closely intertwined with autophagy and mutually cross-regulated is the unfolded protein response (UPR), which is induced by endoplasmic reticulum (ER) stress. Genes involved in the UPR (XBP1, ORMDL3) have also been genetically associated with Crohn's disease and ulcerative colitis. Moreover, the intestinal epithelium at the interface between host and microbe appears particularly affected by IBD-associated hypomorphic function of autophagy and the UPR. The functional convergence of main genetic risk factors for IBD on these innate immune pathways has hence important implications for the host's interaction with the microbiota. Moreover, the genetic convergence on these molecular mechanisms may open novel therapeutic options for IBD that deserve further exploration.
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.