ArticleAmerican journal of respiratory cell and molecular biology2014
Dimethylarginine dimethylaminohydrolase II overexpression attenuates LPS-mediated lung leak in acute lung injury.
Article in American journal of respiratory cell and molecular biology, 2014. 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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The trial behind it
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Who cites it
29 citing papers in PubMed, 41 citations in OpenAlex.
- Endothelial and cardiac dysfunction in long COVID With cardiovascular symptoms is associated with imbalance in the ADMA-DDAH-NOx pathway.Frontiers in cardiovascular medicine · 2026Article
- Mitochondria at the Heart of Sepsis: Mechanisms, Metabolism, and Sex Differences.International journal of molecular sciences · 2025Review
- Adipose-derived stem cells ameliorate radiation-induced lung injury by activating the DDAH1/ADMA/eNOS signaling pathway.Regenerative therapy · 2024Article
- The role of asymmetric dimethylarginine (ADMA) in COVID-19: association with respiratory failure and predictive role for outcome.Scientific reports · 2023Article
- A multicentric consortium study demonstrates that dimethylarginine dimethylaminohydrolase 2 is not a dimethylarginine dimethylaminohydrolase.Nature communications · 2023Article
- Time-Dependent Oxidative Alterations in Plasma and Lung Tissue after Meconium Aspiration in a Rabbit Model.Antioxidants (Basel, Switzerland) · 2022Article
- Divergent Dimethylarginine Dimethylaminohydrolase Isoenzyme Expression in the Central Nervous System.Cellular and molecular neurobiology · 2022Article
- A new perspective on NO pathway in sepsis and ADMA lowering as a potential therapeutic approach.Critical care (London, England) · 2022Review
- An activation specific anti-Mac-1 designed ankyrin repeat protein improves survival in a mouse model of acute lung injury.Scientific reports · 2022Article
- Loss of SOX18/CLAUDIN5 disrupts the pulmonary endothelial barrier in ventilator-induced lung injury.Frontiers in physiology · 2022Article
- A Therapeutic Extracorporeal Device for Specific Removal of Pathologic Asymmetric Dimethylarginine from the Blood.Blood purification · 2022Article
- Inhibition of Class IIa HDACs improves endothelial barrier function in endotoxin-induced acute lung injury.Journal of cellular physiology · 2021Article
- Protective function of DJ-1/PARK7 in lipopolysaccharide and ventilator-induced acute lung injury.Redox biology · 2021Article
- Fibroblast growth factor-2 alleviates the capillary leakage and inflammation in sepsis.Molecular medicine (Cambridge, Mass.) · 2020Article
- Adenosine and ATPγS protect against bacterial pneumonia-induced acute lung injury.Scientific reports · 2020Article
- Biomechanical Forces and Oxidative Stress: Implications for Pulmonary Vascular Disease.Antioxidants & redox signaling · 2019Review
- Inhibition of Dimethylarginine Dimethylaminohydrolase (DDAH) Enzymes as an Emerging Therapeutic Strategy to Target Angiogenesis and Vasculogenic Mimicry in Cancer.Frontiers in oncology · 2019Review
- Penehyclidine Hydrochloride Decreases Pulmonary Microvascular Endothelial Inflammatory Injury Through a Beta-Arrestin-1-Dependent Mechanism.Inflammation · 2018Article
- LPS-induced Acute Lung Injury Involves NF-κB-mediated Downregulation of SOX18.American journal of respiratory cell and molecular biology · 2018Article
- Site-specific and endothelial-mediated dysfunction of the alveolar-capillary barrier in response to lipopolysaccharides.Journal of cellular and molecular medicine · 2018Article
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Authors and funding
14 authors at 1 institution in 2 countries.
Funding
Abstract
Acute lung injury (ALI) is a severe hypoxemic respiratory insufficiency associated with lung leak, diffuse alveolar damage, inflammation, and loss of lung function. Decreased dimethylaminohydrolase (DDAH) activity and increases in asymmetric dimethylarginine (ADMA), together with exaggerated oxidative/nitrative stress, contributes to the development of ALI in mice exposed to LPS. Whether restoring DDAH function and suppressing ADMA levels can effectively ameliorate vascular hyperpermeability and lung injury in ALI is unknown, and was the focus of this study. In human lung microvascular endothelial cells, DDAH II overexpression prevented the LPS-dependent increase in ADMA, superoxide, peroxynitrite, and protein nitration. DDAH II also attenuated the endothelial barrier disruption associated with LPS exposure. Similarly, in vivo, we demonstrated that the targeted overexpression of DDAH II in the pulmonary vasculature significantly inhibited the accumulation of ADMA and the subsequent increase in oxidative/nitrative stress in the lungs of mice exposed to LPS. In addition, augmenting pulmonary DDAH II activity before LPS exposure reduced lung vascular leak and lung injury and restored lung function when DDAH activity was increased after injury. Together, these data suggest that enhancing DDAH II activity may prove a useful adjuvant therapy to treat patients with ALI.
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