ArticleThe Journal of clinical investigation2014
Carbon monoxide-based therapy ameliorates acute pancreatitis via TLR4 inhibition.
Article in The Journal of clinical investigation, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
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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
43 citing papers in PubMed, 77 citations in OpenAlex.
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- Integrative Analysis of Transcriptomics and Metabolomics Reveals the Effects of Western-Style Diets on Spleen Function.Biology · 2025Article
- Mitigating Tumor Recurrence through Mitochondrial Metabolism Inhibition: A Novel NIR Laser-Induced Therapeutic Strategy.Biological procedures online · 2025Article
- Identification of novel amino acid variants in the Han Chinese population that impair toll-like receptor 4 signaling and confer hyporesponsiveness to lipopolysaccharide.Frontiers in immunology · 2025Article
- Oxidative stress, DAMPs, and immune cells in acute pancreatitis: molecular mechanisms and therapeutic prospects.Frontiers in immunology · 2025Review
- From pancreas to lungs: The role of immune cells in severe acute pancreatitis and acute lung injury.Immunity, inflammation and disease · 2024Review
- Nicotinamide adenine dinucleotide phosphate oxidase in pancreatic diseases: Mechanisms and future perspectives.World journal of gastroenterology · 2024Review
- Toll-like receptor 4 in pancreatic damage and immune infiltration in acute pancreatitis.Frontiers in immunology · 2024Review
- Immune Regulation of Heme Oxygenase-1 in Allergic Airway Inflammation.Antioxidants (Basel, Switzerland) · 2022Review
- Circulating monocytes in acute pancreatitis.Frontiers in immunology · 2022Review
- Contributions of HO-1-Dependent MAPK to Regulating Intestinal Barrier Disruption.Biomolecules & therapeutics · 2021Article
- Carbon Monoxide in Pancreatic Islet Transplantation: A New Therapeutic Alternative to Patients With Severe Type 1 Diabetes Mellitus.Frontiers in pharmacology · 2021Review
- Docosahexaenoic Acid Induces Expression of NAD(P)H: Quinone Oxidoreductase and Heme Oxygenase-1 through Activation of Nrf2 in Cerulein-Stimulated Pancreatic Acinar Cells.Antioxidants (Basel, Switzerland) · 2020Article
- Single immunoglobulin and Toll‑interleukin‑1 receptor domain containing molecule protects against severe acute pancreatitis in vitro by negatively regulating the Toll‑like receptor‑4 signaling pathway: A clinical and experimental study.Molecular medicine reports · 2020Article
- Macrophage phenotypic switch orchestrates the inflammation and repair/regeneration following acute pancreatitis injury.EBioMedicine · 2020Article
- NLRP3 Inflammasome-Mediated Inflammation in Acute Pancreatitis.International journal of molecular sciences · 2020Review
- Systemic vasoprotection by inhaled carbon monoxide is mediated through prolonged alterations in monocyte/macrophage function.Nitric oxide : biology and chemistry · 2020Article
- Article
- Carbon Monoxide Releasing Molecule-2-Upregulated ROS-Dependent Heme Oxygenase-1 Axis Suppresses Lipopolysaccharide-Induced Airway Inflammation.International journal of molecular sciences · 2019Article
- Carbon monoxide releasing molecule‑2 (CORM‑2)‑liberated CO ameliorates acute pancreatitis.Molecular medicine reports · 2019Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The protective role of hemeoxygenase-1 (HO-1) in various inflammatory conditions is mediated in part by its products, carbon monoxide (CO) and biliverdin. Here we investigated a therapeutic role for CO and CO-primed cells in acute pancreatitis (AP). In a mouse model of AP, treatment with CO-releasing molecule-2 (CORM-2) decreased mortality, pancreatic damage, and lung injury. CORM-2 decreased systemic inflammatory cytokines, suppressed systemic and pancreatic macrophage TNF-α secretion, and inhibited macrophage TLR4 receptor complex expression. In both human and mouse cells, CORM-2 inhibited endogenous and exogenous ligand-dependent TLR4 activation, which indicates that CORM-2 could be therapeutic for both early and late stages of AP, which involve sterile- and endotoxin-mediated inflammation, respectively. Mice engrafted with TLR4-deficient hematopoietic cells were protected against caerulein-induced AP. In the absence of leukocyte TLR4 expression, CORM-2 did not confer additional protection, which indicates that CORM-2-dependent effects are mediated via suppression of macrophage TLR4 activation. We determined that CO was directly responsible for the protective effects of CORM-2 in AP, as inactive forms of CORM-2 were ineffective. Importantly, adoptive transfer of CORM-2-primed cells reduced AP. Such a therapeutic approach would translate the beneficial effects of CO-based therapies, avoiding CO- or CO-RM-mediated toxicities in AP and a wide range of diseases.
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Registered trials
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