ArticlePloS one2013
Enhanced synthesis and diminished degradation of hydrogen sulfide in experimental colitis: a site-specific, pro-resolution mechanism.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 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
41 citing papers in PubMed, 73 citations in OpenAlex.
- A proof-of-concept, Phase 2 clinical trial of the gastrointestinal safety of a hydrogen sulfide-releasing anti-inflammatory drug.British journal of pharmacology · 2020Trial
- Hydrogen sulfide rescues IFNγ/TNFα-induced intestinal epithelial barrier dysfunction by enhancing oxidative phosphorylation.Scientific reports · 2026Article
- The Janus Face of Oxidative Stress and Hydrogen Sulfide: Insights into Neurodegenerative Disease Pathogenesis.Antioxidants (Basel, Switzerland) · 2025Review
- The reverse transsulfuration pathway affects the colonic microbiota and contributes to colitis in mice.Amino acids · 2024Article
- Cystathionine Gamma-Lyase Regulates TNF-α-Mediated Injury Response in Human Colonic Epithelial Cells and Colonoids.Antioxidants (Basel, Switzerland) · 2024Article
- Chemistry of Hydrogen Sulfide-Pathological and Physiological Functions in Mammalian Cells.Cells · 2023Review
- Role of Hydrogen Sulfide in Inflammatory Bowel Disease.Antioxidants (Basel, Switzerland) · 2023Review
- Hydrogen Sulfide-Releasing Indomethacin-Derivative (ATB-344) Prevents the Development of Oxidative Gastric Mucosal Injuries.Antioxidants (Basel, Switzerland) · 2023Article
- Mechanism-based and computational modeling of hydrogen sulfide biogenesis inhibition: interfacial inhibition.Scientific reports · 2023Article
- Differential Roles of Cystathionine Gamma-Lyase and Mercaptopyruvate Sulfurtransferase in Hapten-Induced Colitis and Contact Dermatitis in Mice.International journal of molecular sciences · 2023Article
- Article
- Hydrogen Sulfide Metabolizing Enzymes in the Intestinal Mucosa in Pediatric and Adult Inflammatory Bowel Disease.Antioxidants (Basel, Switzerland) · 2022Article
- MPST deficiency promotes intestinal epithelial cell apoptosis and aggravates inflammatory bowel disease via AKT.Redox biology · 2022Article
- Detoxification, Hydrogen Sulphide Metabolism and Wound Healing Are the Main Functions That Differentiate Caecum Protein Expression from Ileum of Week-Old Chicken.Animals : an open access journal from MDPI · 2021Article
- Article
- The Role of HAdvances in experimental medicine and biology · 2021Article
- Enhanced Analgesic Effects and Gastrointestinal Safety of a Novel, Hydrogen Sulfide-Releasing Anti-Inflammatory Drug (ATB-352): A Role for Endogenous Cannabinoids.Antioxidants & redox signaling · 2020Article
- The HFrontiers in pharmacology · 2019Article
- HInflammopharmacology · 2018Article
- Chemical Biology of HChemical reviews · 2018Review
Corrections and comments
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Authors and funding
4 authors at 4 institutions in 1 country.
Funding
Abstract
Hydrogen sulfide (H₂S) is produced throughout the gastrointestinal tract, and it contributes to maintenance of mucosal integrity, resolution of inflammation, and repair of damaged tissue. H₂S synthesis is elevated in inflamed and damaged colonic tissue, but the enzymatic sources of that synthesis are not completely understood. In the present study, the contributions of three enzymatic pathways to colonic H₂S synthesis were determined, with tissues taken from healthy rats and rats with colitis. The ability of the colonic tissue to inactivate H₂S was also determined. Colonic tissue from rats with hapten-induced colitis produced significantly more H₂S than tissue from healthy controls. The largest source of the H₂S synthesis was the pathway involving cysteine amino transferase and 3-mercaptopyruvate sulfurtransferase (an α-ketoglutarate-dependent pathway). Elevated H₂S synthesis occurred specifically at sites of mucosal ulceration, and was not related to the extent of granulocyte infiltration into the tissue. Inactivation of H₂S by colonic tissue occurred rapidly, and was significantly reduced at sites of mucosal ulceration. This correlated with a marked decrease in the expression of sulfide quinone reductase in these regions. Together, the increased production and decreased inactivation of H₂S at sites of mucosal ulceration would result in higher H₂S levels at these sites, which promotes of resolution of inflammation and repair of damaged tissue.
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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.