ArticleRespiratory research2010
The cationic amino acid transporter 2 is induced in inflammatory lung models and regulates lung fibrosis.
Article in Respiratory research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 27 citations in OpenAlex.
- RIPK3 Orchestrates Scar-Associated Macrophage Dysfunction to Drive Pulmonary Fibrosis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Solute Carrier transporters in tumor metabolism and immune modulation: implications for therapy.Journal of translational medicine · 2026Review
- Macrophage metabolic reprogramming in sepsis-associated acute lung injury: mechanisms and therapeutic strategies.Frontiers in immunology · 2026Review
- Metabolic dysregulation in pulmonary fibrosis: insights into amino acid contributions and therapeutic potential.Cell death discovery · 2025Review
- The mechanism of gut-lung axis in pulmonary fibrosis.Frontiers in cellular and infection microbiology · 2024Review
- Metabolic reprogramming of pulmonary fibrosis.Frontiers in pharmacology · 2022Review
- Gut microbiome and metabolites: The potential key roles in pulmonary fibrosis.Frontiers in microbiology · 2022Review
- Amino acid transporters as tetraspanin TM4SF5 binding partners.Experimental & molecular medicine · 2020Review
- Metabolic Modulation in Macrophage Effector Function.Frontiers in immunology · 2018Review
- Expression Profile of Cationic Amino Acid Transporters in Rats with Endotoxin-Induced Uveitis.Mediators of inflammation · 2016Article
- Metabolism via Arginase or Nitric Oxide Synthase: Two Competing Arginine Pathways in Macrophages.Frontiers in immunology · 2014Review
- Deletion of cationic amino acid transporter 2 exacerbates dextran sulfate sodium colitis and leads to an IL-17-predominant T cell response.American journal of physiology. Gastrointestinal and liver physiology · 2013Article
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Authors and funding
5 authors at 4 institutions in 1 country.
Funding
Abstract
backgroundArginine is an amino acid that serves as a substrate for the enzymes nitric oxide synthase (NOS) and arginase, leading to synthesis of NO and ornithine, respectively. As such, arginine has the potential to influence diverse fundamental processes in the lung.
methodsWe used mice deficient in cationic amino acid transporter (CAT) 2 in models of allergic airway inflammation and pulmonary fibrosis.
resultsWe report that the arginine transport protein CAT2 was over-expressed in the lung during the induction of allergic airway inflammation. Furthermore, CAT2 mRNA was strongly induced by transgenically over-expressed IL-4, and allergen-induced expression was dependent upon signal-transducer-and-activator-of-transcription (STAT) 6. In situ mRNA hybridization demonstrated marked staining of CAT2, predominantly in scattered mononuclear cells. Analysis of allergic airway inflammation and bleomycin-induced inflammation in CAT2-deficient mice revealed that while inflammation was independent of CAT2 expression, bleomycin-induced fibrosis was dependent upon CAT2. Mechanistic analysis revealed that arginase activity in macrophages was partly dependent on CAT2.
conclusionTaken together, these results identify CAT2 as a regulator of fibrotic responses in the lung.
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