ArticleFrontiers in immunology2013
Arginase 1: an unexpected mediator of pulmonary capillary barrier dysfunction in models of acute lung injury.
Article in Frontiers in immunology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 37 citations in OpenAlex.
- Deciphering the therapeutic mechanisms of Qingfei Litan prescription in acute lung injury: an integrated framework of UHPLC-MS/MS, systems pharmacology, machine learning, andFrontiers in cellular and infection microbiology · 2026Article
- Targeting Arginine Metabolism in Immune Cells for the Treatment of Pulmonary Inflammatory Diseases.Current allergy and asthma reports · 2025Review
- Cardiopulmonary bypass with deep hypothermic circulatory arrest results in organ-specific transcriptomic responses in pediatric swine.Translational research : the journal of laboratory and clinical medicine · 2025Article
- Functional heterogeneity of mesenchymal stem cells and their therapeutic potential in the K18-hACE2 mouse model of SARS-CoV-2 infection.Stem cell research & therapy · 2025Article
- Herbal and Dietary Supplements as Adjunctive Treatment for Mild SARS-CoV-2 Infection in Italy.Nutrients · 2025Review
- Lung macrophages in pulmonary homeostasis and disease: from basic biology to clinical applications.Central-European journal of immunology · 2025Review
- Advantages and disadvantages of treatment of experimental ARDS by M2-polarized RAW 264.7 macrophages.Heliyon · 2023Article
- Not all vaping is the same: differential pulmonary effects of vaping cannabidiol versus nicotine.Thorax · 2023Article
- Proteomics analysis of lung tissue reveals protein makers for the lung injury of adjuvant arthritis rats.Molecular medicine reports · 2023Article
- What Is the Place of Intermediate Care Unit in Patients with COVID-19? A Single Center Experience.International journal of clinical practice · 2023Article
- Combining L-Arginine with vitamin C improves long-COVID symptoms: The LINCOLN Survey.Pharmacological research · 2022Article
- Novel Therapeutics for Diabetic Retinopathy and Diabetic Macular Edema: A Pathophysiologic Perspective.Frontiers in physiology · 2022Review
- l-Arginine and COVID-19: An Update.Nutrients · 2021Review
- Implications of SARS-Cov-2 infection on eNOS and iNOS activity: Consequences for the respiratory and vascular systems.Nitric oxide : biology and chemistry · 2021Review
- Machine Learning-Based Discovery of a Gene Expression Signature in Pediatric Acute Respiratory Distress Syndrome.Critical care explorations · 2021Article
- Dichotomous Role of Tumor Necrosis Factor in Pulmonary Barrier Function and Alveolar Fluid Clearance.Frontiers in physiology · 2021Review
- Myeloid arginase-1 controls excessive inflammation and modulates T cell responses in Pseudomonas aeruginosa pneumonia.Immunobiology · 2021Article
- Severe COVID-19 Is Characterized by an Impaired Type I Interferon Response and Elevated Levels of Arginase Producing Granulocytic Myeloid Derived Suppressor Cells.Frontiers in immunology · 2021Observational
- The effects of the M2a macrophage-induced axonal regeneration of neurons by arginase 1.Bioscience reports · 2020Article
- Complexes of Oligoribonucleotides with d-Mannitol Modulate the Innate Immune Response to Influenza A Virus H1N1 (A/FM/1/47) In Vivo.Pharmaceuticals (Basel, Switzerland) · 2018Article
Corrections and comments
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Authors and funding
11 authors at 4 institutions in 2 countries.
Funding
Abstract
The integrity of epithelial and endothelial barriers in the lower airspaces of the lungs has to be tightly regulated, in order to prevent leakage and to assure efficient gas exchange between the alveoli and capillaries. Both G(-) and G(+) bacterial toxins, such as lipopolysaccharide and pneumolysin, respectively, can be released in high concentrations within the pulmonary compartments upon antibiotic treatment of patients suffering from acute respiratory distress syndrome (ARDS) or severe pneumonia. These toxins are able to impair endothelial barrier function, either directly, or indirectly, by induction of pro-inflammatory mediators and neutrophil sequestration. Toxin-induced endothelial hyperpermeability can involve myosin light chain phosphorylation and/or microtubule rearrangement. Endothelial nitric oxide synthase (eNOS) was proposed to be a guardian of basal barrier function, since eNOS knock-out mice display an impaired expression of inter-endothelial junction proteins and as such an increased vascular permeability, as compared to wild type mice. The enzyme arginase, the activity of which can be regulated by the redox status of the cell, exists in two isoforms - arginase 1 (cytosolic) and arginase 2 (mitochondrial) - both of which can be expressed in lung microvascular endothelial cells. Upon activation, arginase competes with eNOS for the substrate l-arginine, as such impairing eNOS-dependent NO generation and promoting reactive oxygen species generation by the enzyme. This mini-review will discuss recent findings regarding the interaction between bacterial toxins and arginase during acute lung injury and will as such address the role of arginase in bacterial toxin-induced pulmonary endothelial barrier dysfunction.
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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.