ArticleVascular pharmacology
Mechanisms of nitric oxide synthase uncoupling in endotoxin-induced acute lung injury: role of asymmetric dimethylarginine.
Article in Vascular pharmacology. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 54 citations in OpenAlex.
- Control of inflammatory lung injury and repair by metabolic signaling in endothelial cells.Current opinion in hematology · 2025Review
- Dimethylarginine dimethylaminohydrolase 1 protects PMParticle and fibre toxicology · 2022Article
- A new perspective on NO pathway in sepsis and ADMA lowering as a potential therapeutic approach.Critical care (London, England) · 2022Review
- Redox Balance in β-Thalassemia and Sickle Cell Disease: A Love and Hate Relationship.Antioxidants (Basel, Switzerland) · 2022Review
- Sickle Cell Disease: Role of Oxidative Stress and Antioxidant Therapy.Antioxidants (Basel, Switzerland) · 2021Review
- Biomechanical Forces and Oxidative Stress: Implications for Pulmonary Vascular Disease.Antioxidants & redox signaling · 2019Review
- Inhibition of interleukin-6 trans-signaling prevents inflammation and endothelial barrier disruption in retinal endothelial cells.Experimental eye research · 2019Article
- Multiorgan Development of Oxidative and Nitrosative Stress in LPS-Induced Endotoxemia in C57Bl/6 Mice: DHE-BasedOxidative medicine and cellular longevity · 2019Article
- LPS-induced Acute Lung Injury Involves NF-κB-mediated Downregulation of SOX18.American journal of respiratory cell and molecular biology · 2018Article
- Regulation of iNOS-Derived ROS Generation by HSP90 and Cav-1 in Porcine Reproductive and Respiratory Syndrome Virus-Infected Swine Lung Injury.Inflammation · 2017Article
- Perioperative "remote" acute lung injury: recent update.Journal of biomedical research · 2017Article
- Hyper-activation of pp60Free radical biology & medicine · 2017Article
- ROS Signaling in the Pathogenesis of Acute Lung Injury (ALI) and Acute Respiratory Distress Syndrome (ARDS).Advances in experimental medicine and biology · 2017Article
- Tetrahydrobiopterin Protects Against Hypertrophic Heart Disease Independent of Myocardial Nitric Oxide Synthase Coupling.Journal of the American Heart Association · 2016Article
- Role of pulmonary microvascular endothelial cell apoptosis in murine sepsis-induced lung injury in vivo.Respiratory research · 2015Article
- Endothelial nitric oxide synthase deficient mice are protected from lipopolysaccharide induced acute lung injury.PloS one · 2015Article
- Dimethylarginine dimethylaminohydrolase II overexpression attenuates LPS-mediated lung leak in acute lung injury.American journal of respiratory cell and molecular biology · 2014Article
- Dimethylarginine dimethylaminohydrolase (DDAH) overexpression attenuates agricultural organic dust extract-induced inflammation.Journal of environmental immunology and toxicology · 2014Article
- Reactive oxygen species in inflammation and tissue injury.Antioxidants & redox signaling · 2014Review
- Lipopolysaccharide-induced lung injury involves the nitration-mediated activation of RhoA.The Journal of biological chemistry · 2014Article
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
Abstract
Acute lung injury (ALI) is associated with severe alterations in lung structure and function and is characterized by hypoxemia, pulmonary edema, low lung compliance and widespread capillary leakage. Asymmetric dimethylarginine (ADMA), a known cardiovascular risk factor, has been linked to endothelial dysfunction and the pathogenesis of a number of cardiovascular diseases. However, the role of ADMA in the pathogenesis of ALI is less clear. ADMA is metabolized via hydrolytic degradation to l-citrulline and dimethylamine by the enzyme, dimethylarginine dimethylaminohydrolase (DDAH). Recent studies suggest that lipopolysaccharide (LPS) markedly increases the level of ADMA and decreases DDAH activity in endothelial cells. Thus, the purpose of this study was to determine if alterations in the ADMA/DDAH pathway contribute to the development of ALI initiated by LPS-exposure in mice. Our data demonstrate that LPS exposure significantly increases ADMA levels and this correlates with a decrease in DDAH activity but not protein levels of either DDAH I or DDAH II isoforms. Further, we found that the increase in ADMA levels cause an early decrease in nitric oxide (NO(x)) and a significant increase in both NO synthase (NOS)-derived superoxide and total nitrated lung proteins. Finally, we found that decreasing peroxynitrite levels with either uric acid or Manganese (III) tetrakis (1-methyl-4-pyridyl) porphyrin (MnTymPyp) significantly attenuated the lung leak associated with LPS-exposure in mice suggesting a key role for protein nitration in the progression of ALI. In conclusion, this is the first study that suggests a role of the ADMA/DDAH pathway during the development of ALI in mice and that ADMA may be a novel therapeutic biomarker to ascertain the risk for development of ALI.
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