ArticleKidney international2014
Asymmetric dimethylarginine accumulates in the kidney during ischemia/reperfusion injury.
Article in Kidney international, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 48 citations in OpenAlex.
- Untangling amino acid metabolism in renal diseases: mechanisms, dysregulation, and critical gaps.Clinical kidney journal · 2026Review
- Asymmetric Dimethylarginine: A Never-Aging Story.Hormone and metabolic research = Hormon- und Stoffwechselforschung = Hormones et metabolisme · 2025Review
- Ablation of macrophage transcriptional factor FoxO1 protects against ischemia-reperfusion injury-induced acute kidney injury.Acta pharmaceutica Sinica. B · 2025Article
- Cytomegalovirus reactivation and acute and chronic complications in children with cerebral malaria: a prospective cohort study.Malaria journal · 2025Article
- Arginine methyltransferase PRMT1 promotes ferroptosis through EGR1/GLS2 axis in sepsis-related acute lung injury.Communications biology · 2025Article
- Article
- Biomarkers of Arginine Methylation in Diabetic Nephropathy: Novel Insights from Bioinformatics Analysis.Diabetes, metabolic syndrome and obesity : targets and therapy · 2024Article
- A multicentric consortium study demonstrates that dimethylarginine dimethylaminohydrolase 2 is not a dimethylarginine dimethylaminohydrolase.Nature communications · 2023Article
- Nanodrugs alleviate acute kidney injury: Manipulate RONS at kidney.Bioactive materials · 2023Review
- Protein arginine methyltransferases in renal development, injury, repair, and fibrosis.Frontiers in pharmacology · 2023Review
- Role of ADMA in the pathogenesis of microvascular complications in type 2 diabetes mellitus.Frontiers in endocrinology · 2023Review
- An Untargeted Metabolomics Approach on Carfilzomib-Induced Nephrotoxicity.Molecules (Basel, Switzerland) · 2022Article
- A new perspective on NO pathway in sepsis and ADMA lowering as a potential therapeutic approach.Critical care (London, England) · 2022Review
- A Recombinant Dimethylarginine Dimethylaminohydrolase-1-Based Biotherapeutics to Pharmacologically Lower Asymmetric Dimethyl Arginine, thus Improving Postischemic Cardiac Function and Cardiomyocyte Mitochondrial Activity.Molecular pharmacology · 2022Article
- A Therapeutic Extracorporeal Device for Specific Removal of Pathologic Asymmetric Dimethylarginine from the Blood.Blood purification · 2022Article
- Effect of a Low Dose of Carvedilol on Cyclophosphamide-Induced Urinary Toxicity in Rats-A Comparison with Mesna.Pharmaceuticals (Basel, Switzerland) · 2021Article
- Multiple inducers of endothelial NOS (eNOS) dysfunction in sickle cell disease.American journal of hematology · 2021Review
- DDAH-1, via regulation of ADMA levels, protects against ischemia-induced blood-brain barrier leakage.Laboratory investigation; a journal of technical methods and pathology · 2021Article
- Specific Lowering of Asymmetric Dimethylarginine by Pharmacological Dimethylarginine Dimethylaminohydrolase Improves Endothelial Function, Reduces Blood Pressure and Ischemia-Reperfusion Injury.The Journal of pharmacology and experimental therapeutics · 2021Article
- The Functional Polymorphism ofFrontiers in cardiovascular medicine · 2021Article
Corrections and comments
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Authors and funding
14 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ischemia/reperfusion injury is the leading cause of acute tubular necrosis. Nitric oxide has a protective role against ischemia/reperfusion injury; however, the role of asymmetric dimethylarginine (ADMA), an endogenous inhibitor of nitric oxide synthase, in ischemia/reperfusion injury remains unclear. ADMA is produced by protein arginine methyltransferase (PRMT) and is mainly degraded by dimethylarginine dimethylaminohydrolase (DDAH). Here we examined the kinetics of ADMA and PRMT and DDAH expression in the kidneys of ischemia/reperfusion-injured mice. After the injury, DDAH-1 levels were decreased and renal and plasma ADMA values were increased in association with renal dysfunction. Renal ADMA was correlated with 8-hydroxy-2'-deoxyguanosine, a marker of oxidative stress. An antioxidant, N-acetylcysteine, or a proteasomal inhibitor, MG-132, restored these alterations. Infusion of subpressor dose of ADMA exacerbated renal dysfunction, capillary loss, and tubular necrosis in the kidneys of ischemia/reperfusion-injured wild mice, while damage was attenuated in DDAH transgenic mice. Thus, ischemia/reperfusion injury-induced oxidative stress may reduce DDAH expression and cause ADMA accumulation, which may contribute to capillary loss and tubular necrosis in the kidney.
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