ReviewSeminars in immunopathology2013
The unfolded protein response and gastrointestinal disease.
Review in Seminars in immunopathology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
44 citing papers in PubMed, 86 citations in OpenAlex.
- Endoplasmic reticulum stress as a mechanistic link between nutrition and inflammatory bowel disease.Frontiers in nutrition · 2026Review
- Identifying Lactylation-related biomarkers and therapeutic drugs in ulcerative colitis: insights from machine learning and molecular docking.BMC pharmacology & toxicology · 2025Article
- IRE1α and IRE1β Protect Intestinal Epithelium and Suppress Colorectal Tumorigenesis through Distinct Mechanisms.bioRxiv : the preprint server for biology · 2025Article
- Endoplasmic reticulum stress in gut inflammation: Implications for ulcerative colitis and Crohn's disease.World journal of gastroenterology · 2025Review
- Tauroursodeoxycholic Acid (TUDCA) Reduces ER Stress and Lessens Disease Activity in Ulcerative Colitis.medRxiv : the preprint server for health sciences · 2025Article
- Pancreastatin Inhibition Alters the Colonic Epithelial Cells Profile in a Sex-Dependent Manner.International journal of molecular sciences · 2024Article
- Essential roles of the unfolded protein response in intestinal physiology.eGastroenterology · 2024Review
- The IRE1α/XBP1 pathway sustains cytokine responses of group 3 innate lymphoid cells in inflammatory bowel disease.The Journal of clinical investigation · 2024Article
- Active polypeptide MDANP protect against necrotizing enterocolitis (NEC) by regulating the PERK-eIF2ɑ-QRICH1 axis.Scientific reports · 2023Article
- Review
- Therapeutic interventions target the NLRP3 inflammasome in ulcerative colitis: Comprehensive study.World journal of gastroenterology · 2023Review
- Depletion of chop suppresses procedural apoptosis and enhances innate immunity in loach Misgurnus anguillicaudatus under ammonia nitrogen stress.Journal of animal science · 2023Article
- Identifying Macrophage-Related Genes in Ulcerative Colitis Using Weighted Coexpression Network Analysis and Machine Learning.Mediators of inflammation · 2023Article
- Pharmacological targeting of endoplasmic reticulum stress in disease.Nature reviews. Drug discovery · 2022Review
- Cold Exposure Induces Intestinal Barrier Damage and Endoplasmic Reticulum Stress in the ColonFrontiers in physiology · 2022Article
- Expression profiling of ileal mucosa in asthma reveals upregulation of innate immunity and genes characteristic of Paneth and goblet cells.Allergy, asthma, and clinical immunology : official journal of the Canadian Society of Allergy and Clinical Immunology · 2021Article
- Review
- Ulcerative colitis.Nature reviews. Disease primers · 2020Review
- Review
- Grass carp (Ctenopharyngodon idella) NRF2 alleviates the oxidative stress and enhances cell viability through upregulating the expression of HO-1.Fish physiology and biochemistry · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 3 institutions in 2 countries.
Funding
Abstract
As the inner lining of the gastrointestinal tract, the intestinal epithelium serves an essential role in innate immune function at the interface between the host and microbiota. Given the unique environmental challenges and thus physiologic secretory functions of this surface, it is exquisitely sensitive to perturbations that affect its capacity to resolve endoplasmic reticulum (ER) stress. Genetic deletion of factors involved in the unfolded protein response (UPR), which functions in the resolution of ER stress that arises from misfolded proteins, result in spontaneous intestinal inflammation closely mimicking human inflammatory bowel disease (IBD). This is demonstrated by observations wherein deletion of genes such as Xbp1 and Agr2 profoundly affects the intestinal epithelium and results in spontaneous intestinal inflammation. Moreover, both genes, along with others (e.g., ORDML3) represent genetic risk factors for human IBD, both Crohn's disease and ulcerative colitis. Here, we review the current mechanistic understanding for how unresolved ER stress can lead to intestinal inflammation and highlight the findings that implicate ER stress as a genetically affected biological pathway in IBD. We further discuss environmental and microbial factors that might impact on the epithelium's capacity to resolve ER stress and which may constitute exogenous factors that may precipitate disease in genetically susceptible individuals.
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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.