ArticleScientific reports2017
GSTO1-1 plays a pro-inflammatory role in models of inflammation, colitis and obesity.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers, 1 of them a synthesis that pooled it.
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Who cites it
31 citing papers in PubMed, 1 synthesis or guideline pooled it, 64 citations in OpenAlex.
- Regulation of Intestinal Inflammation by Dietary Fats.Frontiers in immunology · 2020Pooled it
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- Adipose Tissue-Derived Small Extracellular Vesicles in Plasma Reveal Molecular Circuitries Underlying Glucose Intolerance.Obesity (Silver Spring, Md.) · 2026Article
- Tissue-Specific Expression of Glutathione-S-Transferase Isoforms in Myelomeningocele: An Immunohistochemical Study.Child's nervous system : ChNS : official journal of the International Society for Pediatric Neurosurgery · 2025Article
- Global proteomic analysis ofmSystems · 2025Article
- The Effect of Circulating Proteins and Their Role in Mediating Adiposity's Effect on Endometrial Cancer Risk: Mendelian Randomization and Colocalization Analyses.Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology · 2025Article
- Glutathione S-transferase omega class 1 (GSTO1)-associated large extracellular vesicles are involved in tumor-associated macrophage-mediated cisplatin resistance in bladder cancer.Molecular oncology · 2024Article
- Regulatory Effects of 198-bp Structural Variants in theInternational journal of molecular sciences · 2024Article
- Comparative transcriptome and methylome of polar bears, giant and red pandas reveal diet-driven adaptive evolution.Evolutionary applications · 2024Article
- Regulation of GlutathioneInternational journal of molecular sciences · 2024Article
- The CLCF1-CNTFR axis drives an immunosuppressive tumor microenvironment and blockade enhances the effects of established cancer therapies.Research square · 2024Article
- Disclosing the molecular profile of the human amniotic mesenchymal stromal cell secretome by filter-aided sample preparation proteomic characterization.Stem cell research & therapy · 2023Article
- Hypusination Maintains Intestinal Homeostasis and Prevents Colitis and Carcinogenesis by Enhancing Aldehyde Detoxification.Gastroenterology · 2023Article
- Inhibition of glutathione S-transferase omega 1-catalyzed protein deglutathionylation suppresses adipocyte differentiation.BMB reports · 2023Article
- Article
- Integrated Covalent Drug Design Workflow Using Site Identification by Ligand Competitive Saturation.Journal of chemical theory and computation · 2023Article
- Development of a Prediction Model for Short-Term Remission of Patients with Crohn's Disease Treated with Anti-TNF Drugs.International journal of molecular sciences · 2023Article
- The Role of Post-Translational Modifications in Regulation of NLRP3 Inflammasome Activation.International journal of molecular sciences · 2023Review
- TheMedicina (Kaunas, Lithuania) · 2023Article
- Editorial: The expanding functional network of glutathione transferases.Frontiers in molecular biosciences · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
19 authors at 8 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Glutathione transferase Omega 1 (GSTO1-1) is an atypical GST reported to play a pro-inflammatory role in response to LPS. Here we show that genetic knockout of Gsto1 alters the response of mice to three distinct inflammatory disease models. GSTO1-1 deficiency ameliorates the inflammatory response stimulated by LPS and attenuates the inflammatory impact of a high fat diet on glucose tolerance and insulin resistance. In contrast, GSTO1-1 deficient mice show a more severe inflammatory response and increased escape of bacteria from the colon into the lymphatic system in a dextran sodium sulfate mediated model of inflammatory bowel disease. These responses are similar to those of TLR4 and MyD88 deficient mice in these models and confirm that GSTO1-1 is critical for a TLR4-like pro-inflammatory response in vivo. In wild-type mice, we show that a small molecule inhibitor that covalently binds in the active site of GSTO1-1 can be used to ameliorate the inflammatory response to LPS. Our findings demonstrate the potential therapeutic utility of GSTO1-1 inhibitors in the modulation of inflammation and suggest their possible application in the treatment of a range of inflammatory conditions.
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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.