ArticleOxidative medicine and cellular longevity2013
Carbon monoxide protects against hepatic ischemia/reperfusion injury via ROS-dependent Akt signaling and inhibition of glycogen synthase kinase 3β.
Article in Oxidative medicine and cellular longevity, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 49 citations in OpenAlex.
- PRKAA2 mediates the pathogenesis of metabolic dysfunction-associated steatotic liver disease via PI3K/AKT signaling pathway.Human genomics · 2025Article
- Carbon Monoxide as a Molecular Modulator of Ischemia-Reperfusion Injury: New Insights for Translational Application in Organ Transplantation.International journal of molecular sciences · 2025Review
- Compelling Evidence: A Critical Update on the Therapeutic Potential of Carbon Monoxide.Medicinal research reviews · 2025Review
- CO confers neuroprotection via activating the PERK-calcineurin pathway and inhibiting necroptosis.Cell death discovery · 2025Article
- Gracillin Protects Liver Ischemia-Reperfusion Injury from Oxidative Stress-Induced Apoptosis.Drug design, development and therapy · 2025Article
- Blackberry-Loaded AgNPs Attenuate Hepatic Ischemia/Reperfusion Injury via PI3K/Akt/mTOR Pathway.Metabolites · 2023Article
- Molecular Regulation of Heme Oxygenase-1 Expression by E2F Transcription Factor 2 in Lung Fibroblast Cells: Relevance to Idiopathic Pulmonary Fibrosis.Biomolecules · 2022Article
- Carbon Monoxide Signaling: Examining Its Engagement with Various Molecular Targets in the Context of Binding Affinity, Concentration, and Biologic Response.Pharmacological reviews · 2022Review
- Role of Glycogen Synthase Kinase-3 in Interferon-γ-Mediated Immune Hepatitis.International journal of molecular sciences · 2022Review
- Regulation of autophagy as a therapeutic option in glioblastoma.Apoptosis : an international journal on programmed cell death · 2021Review
- Carbon monoxide-triggered health effects: the important role of the inflammasome and its possible crosstalk with autophagy and exosomes.Archives of toxicology · 2021Review
- Carbon Monoxide Releasing Molecule-3 Enhances Heme Oxygenase-1 Induction via ROS-Dependent FoxO1 and Nrf2 in Brain Astrocytes.Oxidative medicine and cellular longevity · 2021Article
- The Protective Effects of Carbon Monoxide Against Hepatic Warm Ischemia-Reperfusion Injury in MHC-Inbred Miniature Swine.Journal of gastrointestinal surgery : official journal of the Society for Surgery of the Alimentary Tract · 2020Article
- Carbon Monoxide Being Hydrogen Sulfide and Nitric Oxide Molecular Sibling, as Endogenous and Exogenous Modulator of Oxidative Stress and Antioxidative Mechanisms in the Digestive System.Oxidative medicine and cellular longevity · 2020Review
- Review
- Carbon monoxide attenuates amyloidogenesis via down-regulation of NF-κB-mediated BACE1 gene expression.Aging cell · 2019Article
- Carbon monoxide-induced metabolic switch in adipocytes improves insulin resistance in obese mice.JCI insight · 2018Article
- Carbon monoxide decreases interleukin-1β levels in the lung through the induction of pyrin.Cellular & molecular immunology · 2017Article
- Effect of mild hypothermia preconditioning against low temperature (4°C) induced rat liver cell injury in vitro.PloS one · 2017Article
- Protection of rat liver against hepatic ischemia-reperfusion injury by a novel selenocysteine-containing 7-mer peptide.Molecular medicine reports · 2016Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Carbon monoxide (CO) may exert important roles in physiological and pathophysiological states through the regulation of cellular signaling pathways. CO can protect organ tissues from ischemia/reperfusion (I/R) injury by modulating intracellular redox status and by inhibiting inflammatory, apoptotic, and proliferative responses. However, the cellular mechanisms underlying the protective effects of CO in organ I/R injury remain incompletely understood. In this study, a murine model of hepatic warm I/R injury was employed to assess the role of glycogen synthase kinase-3 (GSK3) and phosphatidylinositol 3-kinase (PI3K)-dependent signaling pathways in the protective effects of CO against inflammation and injury. Inhibition of GSK3 through the PI3K/Akt pathway played a crucial role in CO-mediated protection. CO treatment increased the phosphorylation of Akt and GSK3-beta (GSK3β) in the liver after I/R injury. Furthermore, administration of LY294002, an inhibitor of PI3K, compromised the protective effect of CO and decreased the level of phospho-GSK3β after I/R injury. These results suggest that CO protects against liver damage by maintaining GSK3β phosphorylation, which may be mediated by the PI3K/Akt signaling pathway. Our study provides additional support for the therapeutic potential of CO in organ injury and identifies GSK3β as a therapeutic target for CO in the amelioration of hepatic injury.
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