ReviewFrontiers in immunology2019
Dysregulation of Intestinal Epithelial Cell RIPK Pathways Promotes Chronic Inflammation in the IBD Gut.
Review in Frontiers in immunology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 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
55 citing papers in PubMed, 91 citations in OpenAlex.
- A Randomized Phase I Trial Evaluating Safety and Pharmacokinetics of Single and Multiple Ascending Doses of Eclitasertib, a RIPK1 Inhibitor, in Healthy Participants.Advances in therapy · 2025Trial
- Mechanisms of phosphorylation in colitis regulation: PP2Acα as an emerging therapeutic target for inflammatory bowel disease.Molecular biology reports · 2026Review
- The dual role of RIPK family in IBD: from cell death to therapeutic targeting.Molecular medicine (Cambridge, Mass.) · 2026Review
- Article
- In vitro modeling of inflammatory bowel diseases using a newly developed immunocompetent colon epithelial monolayer co-culture model.npj biomedical innovations · 2026Article
- Pneumococcal Endopeptidase O Attenuates Colitis by Inhibiting the Macrophage-CCL2 Axis and Reshaping Gut Microbiota.Journal of inflammation research · 2026Article
- Intestinal Epithelial-Derived USP13 Alleviates Colonic Inflammation by Suppressing GRP78-mediated Endoplasmic Reticulum Stress.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Colon Dialysis with Yishen Decoction Improves Autophagy Disorder in Intestinal Mucosal Epithelial Cells of Chronic Renal Failure by Regulating SIRT1 Pathway.Chinese journal of integrative medicine · 2025Article
- Validation of the i-Tracker Drug and Total Anti-Drug Antibody CLIA Assays on IDS-iSYS for Therapeutic Drug Monitoring in Adalimumab- and Infliximab-Treated Patients.Diagnostics (Basel, Switzerland) · 2025Article
- MAPK signaling mediated intestinal inflammation induced by endoplasmic reticulum stress and NOD2.Molecular and cellular biochemistry · 2025Article
- A derivative of tanshinone IIA and salviadione, 15a, inhibits inflammation and alleviates DSS-induced colitis in mice by direct binding and inhibition of RIPK2.Acta pharmacologica Sinica · 2025Article
- The Involvement of RIPK1 in Alopecia Areata.International journal of molecular sciences · 2025Article
- Drug Development in Inflammatory Bowel Diseases: What Is Next?Pharmaceuticals (Basel, Switzerland) · 2025Review
- MYO5B and the Polygenic Landscape of Very Early-Onset Inflammatory Bowel Disease in an Ethnically Diverse Population.Inflammatory bowel diseases · 2025Article
- ITLN1 exacerbates Crohn's colitis by driving ZBP1-dependent PANoptosis in intestinal epithelial cells through antagonizing TRIM8-mediated CAPN2 ubiquitination.International journal of biological sciences · 2025Article
- Systemic dysregulation of the gut microenvironment plays a pivotal role in the onset and progression of inflammatory bowel disease.Frontiers in immunology · 2025Review
- Article
- The autophagy protein RUBCNL/PACER represses RIPK1 kinase-dependent apoptosis and necroptosis.Autophagy · 2024Article
- Comparative Study of an Antioxidant Compound and Ethoxyquin on Feed Oxidative Stability and on Performance, Antioxidant Capacity, and Intestinal Health in Starter Broiler Chickens.Antioxidants (Basel, Switzerland) · 2024Article
- Receptor interacting serine/threonine kinase 2 promotes rheumatoid arthritis progression and partially regulates nuclear factor kappa B pathway.CytoJournal · 2024Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Crohn's disease (CD) and ulcerative colitis (UC) are common intestinal bowel diseases (IBD) characterized by intestinal epithelial injury including extensive epithelial cell death, mucosal erosion, ulceration, and crypt abscess formation. Several factors including activated signaling pathways, microbial dysbiosis, and immune deregulation contribute to disease progression. Although most research efforts to date have focused on immune cells, it is becoming increasingly clear that intestinal epithelial cells (IEC) are important players in IBD pathogenesis. Aberrant or exacerbated responses to how IEC sense IBD-associated microbes, respond to TNF stimulation, and regenerate and heal the injured mucosa are critical to the integrity of the intestinal barrier. The role of several genes and pathways in which single nucleotide polymorphisms (SNP) showed strong association with IBD has recently been studied in the context of IEC. In patients with IBD, it has been shown that the expression of specific dysregulated genes in IECs plays an important role in TNF-induced cell death and microbial sensing. Among them, the NF-κB pathway and its target gene TNFAIP3 promote TNF-induced and receptor interacting protein kinase (RIPK1)-dependent intestinal epithelial cell death. On the other hand, RIPK2 functions as a key signaling protein in host defense responses induced by activation of the cytosolic microbial sensors nucleotide-binding oligomerization domain-containing proteins 1 and 2 (NOD1 and NOD2). The RIPK2-mediated signaling pathway leads to the activation of NF-κB and MAP kinases that induce autophagy following infection. This article will review these dysregulated RIPK pathways in IEC and their role in promoting chronic inflammation. It will also highlight future research directions and therapeutic approaches involving RIPKs in IBD.
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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.