ArticleImmunity, inflammation and disease2021
The PI3K pathway as a therapeutic intervention point in inflammatory bowel disease.
Article in Immunity, inflammation and disease, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 30 citations in OpenAlex.
- Potential mechanism of Lactiflorin in treating ulcerative colitis via modulation of the PI3K/AKT pathway: a study integrating network analysis, bioinformatics analysis, and experimental evidence.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Ulcerative colitis: signaling pathways, therapeutic targets and interventional strategies.Signal transduction and targeted therapy · 2026Review
- Pharmacogenomic Pathways Underlying Variable Vedolizumab Response in Crohn's Disease Patients: A Rare-Variant Analysis.Biomedicines · 2026Article
- Network Pharmacology-Metabolomics Integration Reveals the Multiple Targets and Mechanisms of Total Glucosides of Paeony Against Ulcerative Colitis.Journal of inflammation research · 2026Article
- Wenyang Decoction Ameliorates DSS-Induced Ulcerative Colitis by Regulating Macrophage Polarization and the PI3K/AKT/mTOR/HIF-1α Signaling Pathway.Mediators of inflammation · 2026Article
- Clonal Hematopoiesis of Indeterminate Potential in Crohn's Disease and Ulcerative Colitis.Inflammatory bowel diseases · 2025Article
- Molecular Mechanisms and Clinical Aspects of Colitis-Associated Cancer in Ulcerative Colitis.Cells · 2025Review
- Article
- Sphingosine-1-phosphate alleviates colitis by regulating macrophage polarization and PI3k-Akt signaling.Frontiers in immunology · 2025Article
- Underneath the Gut-Brain Axis in IBD-Evidence of the Non-Obvious.International journal of molecular sciences · 2024Review
- Key Disease-Related Genes and Immune Cell Infiltration Landscape in Inflammatory Bowel Disease: A Bioinformatics Investigation.International journal of molecular sciences · 2024Article
- Clonal Hematopoiesis of Indeterminate Potential in Crohn's Disease and Ulcerative Colitis.medRxiv : the preprint server for health sciences · 2024Article
- Stratifying macrophages based on their infectious burden identifies novel host targets for intervention during Crohn's disease associated adherent-invasiveMicrobiology (Reading, England) · 2024Article
- Blockade of PI3K/AKT signaling pathway by Astragaloside IV attenuates ulcerative colitis via improving the intestinal epithelial barrier.Journal of translational medicine · 2024Article
- Feline Chronic Gingivostomatitis Diagnosis and Treatment through Transcriptomic Insights.Pathogens (Basel, Switzerland) · 2024Article
- [Acetylcorynoline relieves 2, 4, 6-trinitrobenesulfonic acid-induced Crohn's disease-like colitis in mice by regulating intestinal epithelial cell apoptosis].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2023Article
- Humanized NSG Mouse Models as a Preclinical Tool for Translational Research in Inflammatory Bowel Diseases.International journal of molecular sciences · 2023Article
- The role of cholesterol and mitochondrial bioenergetics in activation of the inflammasome in IBD.Frontiers in immunology · 2022Review
- LncRNA-miRNA-mRNA Network Analysis Reveals the Potential Biomarkers in Crohn's Disease Rats Treated with Herb-Partitioned Moxibustion.Journal of inflammation research · 2022Article
- The PI3K pathway as a therapeutic intervention point in inflammatory bowel disease.Immunity, inflammation and disease · 2021Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
With glucose being the preferred source of energy in activated T cells, targeting glycolysis has become an attractive therapeutic intervention point for chronic inflammatory bowel diseases (IBD). The switch to glycolysis is mediated by phosphoinositide-3-kinases (PI3K) which relay signals from surface receptors to the AKT pathway. We first confirmed by analysis of the oxygen consumption rate (OCR) and extracellular acidification rate (ECAR) that metabolism is shifted towards glycolysis in IBD patients as compared to non-IBD donors. In contrast to non-IBD donors, OCR correlated with ECAR (IBD: cor = 0.79, p = 2E-10; non-IBD: cor = 0.37, p = n.s.), in IBD patients. Second, we tested the PI3K inhibitor copanlisib as a potential therapeutic. Ex vivo, copanlisib suppressed the ECAR significantly in T cells activated by anti-CD3 antibodies and significantly decreased ECAR rates in the presence of copanlisib (anti-CD3: 58.24 ± 29.06; copanlisib: 43.16 ± 20.23, p < .000. In addition, copanlisib impaired the activation of CD4
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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.