ArticlePloS one2019
Autophagy deficiency exacerbates colitis through excessive oxidative stress and MAPK signaling pathway activation.
Article in PloS one, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 23 citations in OpenAlex.
- Oridonin ameliorates ulcerative colitis by regulating the PI3K/AKT/mTOR signaling pathway to activate autophagy.International journal of molecular medicine · 2026Article
- AXL-dependent autophagy impairment differentiates monocyte-derived macrophages from Crohn's disease and intestinal tuberculosis.Indian journal of gastroenterology : official journal of the Indian Society of Gastroenterology · 2026Article
- Gut microbiota-derived metabolites and IL-22 signaling in inflammatory bowel disease: context-dependent regulation of mucosal repair and inflammation.Frontiers in immunology · 2026Review
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- Involvement of gut microbiota recovery and autophagy induction in Youhua Kuijie formula's protection against experimental ulcerative colitis.Experimental animals · 2024Article
- Autophagy in colitis-associated colon cancer: exploring its potential role in reducing initiation and preventing IBD-Related CAC development.Autophagy · 2024Review
- How autophagy, a potential therapeutic target, regulates intestinal inflammation.Frontiers in immunology · 2023Review
- Perindopril/Ambrosin Combination Mitigates Dextran Sulfate Sodium-Induced Colitis in Mice: Crosstalk between Toll-Like Receptor 4, the Pro-Inflammatory Pathways, and SIRT1/PPAR-γ Signaling.Pharmaceuticals (Basel, Switzerland) · 2022Article
- Procyanidin A1 alleviates DSS-induced ulcerative colitis via regulating AMPK/mTOR/p70S6K-mediated autophagy.Journal of physiology and biochemistry · 2022Article
- The Function of Natural Polysaccharides in the Treatment of Ulcerative Colitis.Frontiers in pharmacology · 2022Review
- Targeting autophagy to overcome drug resistance: further developments.Journal of hematology & oncology · 2020Review
Corrections and comments
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Authors and funding
16 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND AND
aimAutophagy is an essential process involved in the pathogenesis of inflammatory bowel disease (IBD). Although there are many data showing the roles of autophagy in intestinal epithelial cells (IECs), the mechanisms involved remain to be fully elucidated. We investigated the influence of autophagy in IECs on gastrointestinal tract inflammation.
methodsMice with conditional knockout of Atg5 in IECs (Atg5flox/flox/villin-Cre mice) were subjected to dextran sulfate sodium (DSS)-induced colitis and analyzed for colitis susceptibility. Additionally, we used Atg5-silenced rat IECs (IEC6shAtg5 cells) for in vitro assays.
resultsSensitivity to DSS markedly increased in Atg5flox/flox/villin-Cre mice compared to that in wild-type mice. In IEC6shAtg5 cells, apoptosis was enhanced, and cell viability significantly decreased compared to IEC-6 cells. The expression of proinflammatory cytokines increased upon suppression of autophagy. Furthermore, silencing of Atg5 was associated with inflammation of IECs, activation of the mitogen-activated protein kinase (MAPK) signaling pathway by the intracellular reactive oxygen species accumulation, and NF-κB p65 phosphorylation.
conclusionsAutophagy in IECs plays an essential role in the maintenance of intestinal homeostasis, and autophagy deficiency triggers inflammation. Development of methods targeting autophagy might be beneficial in the treatment of IBD.
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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.