ArticleMucosal immunology2014
C/EBP homologous protein inhibits tissue repair in response to gut injury and is inversely regulated with chronic inflammation.
Article in Mucosal immunology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 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.
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Who cites it
21 citing papers in PubMed, 31 citations in OpenAlex.
- Nitrate-mediated luminal expansion ofmBio · 2026Article
- Mitonuclear Communication in Stem Cell Function.Cell proliferation · 2025Review
- Essential roles of the unfolded protein response in intestinal physiology.eGastroenterology · 2024Review
- CHOP-mediated IL-23 overexpression does not drive colitis in experimental spondyloarthritis.Scientific reports · 2024Article
- Intestinal epithelial cell metabolism at the interface of microbial dysbiosis and tissue injury.Mucosal immunology · 2022Review
- Short-Chain Fatty Acid Decreases the Expression of CEBPB to Inhibit miR-145-Mediated DUSP6 and Thus Further Suppresses Intestinal Inflammation.Inflammation · 2022Article
- Curcumin Improves Epithelial Barrier Integrity of Caco-2 Monolayers by Inhibiting Endoplasmic Reticulum Stress and Subsequent Apoptosis.Gastroenterology research and practice · 2021Article
- The Impact of Endoplasmic Reticulum-Associated Protein Modifications, Folding and Degradation on Lung Structure and Function.Frontiers in physiology · 2021Review
- Regulation of Endoplasmic Reticulum Stress-Autophagy: A Potential Therapeutic Target for Ulcerative Colitis.Frontiers in pharmacology · 2021Review
- Article
- Sirtuin 1 alleviates endoplasmic reticulum stress-mediated apoptosis of intestinal epithelial cells in ulcerative colitis.World journal of gastroenterology · 2019Article
- ER Stress and the UPR in Shaping Intestinal Tissue Homeostasis and Immunity.Frontiers in immunology · 2019Review
- Mitochondrial function - gatekeeper of intestinal epithelial cell homeostasis.Nature reviews. Gastroenterology & hepatology · 2018Review
- miR-130a and miR-212 Disrupt the Intestinal Epithelial Barrier through Modulation of PPARγ and Occludin Expression in Chronic Simian Immunodeficiency Virus-Infected Rhesus Macaques.Journal of immunology (Baltimore, Md. : 1950) · 2018Article
- Cellular Stress Responses and Gut Microbiota in Inflammatory Bowel Disease.Gastroenterology research and practice · 2018Review
- Mitochondrial function controls intestinal epithelial stemness and proliferation.Nature communications · 2016Article
- AIM2 contributes to the maintenance of intestinal integrity via Akt and protects against Salmonella mucosal infection.Mucosal immunology · 2016Article
- Article
- Mitochondria Retrograde Signaling and the UPR mt: Where Are We in Mammals?International journal of molecular sciences · 2015Review
- Mechanisms of Microbe-Host Interaction in Crohn's Disease: Dysbiosis vs. Pathobiont Selection.Frontiers in immunology · 2015Review
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 2 countries.
Funding
Abstract
Loss of intestinal epithelial cell (IEC) homeostasis and apoptosis negatively affect intestinal barrier function. Uncontrolled activation of the unfolded protein response (UPR) in IEC contributes to an impaired barrier and is implicated in the pathogenesis of inflammatory bowel diseases. However, the contribution of the UPR target gene C/EBP homologous protein (CHOP), an apoptosis-associated transcription factor, to inflammation-related disease susceptibility remains unclear. Consistent with observations in patients with ulcerative colitis, we show that despite UPR activation in the epithelium, CHOP expression was reduced in mouse models of T-cell-mediated and bacteria-driven colitis. To elucidate the molecular mechanisms of IEC-specific CHOP expression, we generated a conditional transgenic mouse model (Chop(IEC Tg/Tg)). Chop overexpression increased the susceptibility toward dextran sodium sulfate (DSS)-induced intestinal inflammation and mucosal tissue injury. Furthermore, a delayed recovery from DSS-induced colitis and impaired closure of mechanically induced mucosal wounds was observed. Interestingly, these findings seemed to be independent of CHOP-mediated apoptosis. In vitro and in vivo cell cycle analyses rather indicated a role for CHOP in epithelial cell proliferation. In conclusion, these data show that IEC-specific overexpression impairs epithelial cell proliferation and mucosal tissue regeneration, suggesting an important role for CHOP beyond mediating apoptosis.
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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.