ArticleCirculation2009
Vascular endothelial-specific dimethylarginine dimethylaminohydrolase-1-deficient mice reveal that vascular endothelium plays an important role in removing asymmetric dimethylarginine.
Article in Circulation, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.
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Who cites it
46 citing papers in PubMed, 89 citations in OpenAlex.
- The Non-Traditional Cardiovascular Culprits in Chronic Kidney Disease: Mineral Imbalance and Uremic Toxin Accumulation.International journal of molecular sciences · 2025Review
- Sodium tanshinone IIA sulfonate protects vascular relaxation in ApoE-knockout mice by inhibiting the SYK-NLRP3 inflammasome-MMP2/9 pathway.BMC cardiovascular disorders · 2024Article
- DDAH1 Protects against Cardiotoxin-Induced Muscle Injury and Regeneration.Antioxidants (Basel, Switzerland) · 2023Article
- Human pulmonary microvascular endothelial cell DDAH1-mediated nitric oxide production promotes pulmonary smooth muscle cell apoptosis in co-culture.American journal of physiology. Lung cellular and molecular physiology · 2023Article
- Hepatic DDAH1 mitigates hepatic steatosis and insulin resistance in obese mice: Involvement of reduced S100A11 expression.Acta pharmaceutica Sinica. B · 2023Article
- The role of asymmetric dimethylarginine (ADMA) in COVID-19: association with respiratory failure and predictive role for outcome.Scientific reports · 2023Article
- Arginine Dysregulation and Myocardial Dysfunction in a Mouse Model and Children with Chronic Kidney Disease.Nutrients · 2023Article
- Mechanical force promotes dimethylarginine dimethylaminohydrolase 1-mediated hydrolysis of the metabolite asymmetric dimethylarginine to enhance bone formation.Nature communications · 2022Article
- Review
- DDAH1 promoter -396 4N insertion variant is associated with increased risk of type 2 diabetes in a gender-dependent manner.Molecular genetics & genomic medicine · 2020Article
- Heat shock protein 60 regulates yolk sac erythropoiesis in mice.Cell death & disease · 2019Article
- DDAH1 regulates apoptosis and angiogenesis in human fetal pulmonary microvascular endothelial cells.Physiological reports · 2019Article
- Neuropilin-1 maintains dimethylarginine dimethylaminohydrolase 1 expression in endothelial cells, and contributes to protection from angiotensin II-induced hypertension.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019Article
- Asymmetric dimethylarginine (ADMA) as an important risk factor for the increased cardiovascular diseases and heart failure in chronic kidney disease.Nitric oxide : biology and chemistry · 2018Review
- Article
- Restoration of perivascular adipose tissue function in diet-induced obese mice without changing bodyweight.British journal of pharmacology · 2017Article
- Cardiomyocyte dimethylarginine dimethylaminohydrolase-1 (DDAH1) plays an important role in attenuating ventricular hypertrophy and dysfunction.Basic research in cardiology · 2017Article
- Roles of Cells from the Arterial Vessel Wall in Atherosclerosis.Mediators of inflammation · 2017Review
- Asymmetric dimethylarginine (ADMA) elevation and arginase up-regulation contribute to endothelial dysfunction related to insulin resistance in rats and morbidly obese humans.The Journal of physiology · 2016Article
- Dimethylarginine dimethylaminohydrolase-2 deficiency promotes vascular regeneration and attenuates pathological angiogenesis.Experimental eye research · 2016Article
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 2 countries.
Funding
Abstract
backgroundAsymmetrical methylarginines inhibit NO synthase activity and thereby decrease NO production. Dimethylarginine dimethylaminohydrolase 1 (DDAH1) degrades asymmetrical methylarginines. We previously demonstrated that in the heart DDAH1 is predominantly expressed in vascular endothelial cells. Because an earlier study showed that mice with global DDAH1 deficiency experienced embryonic lethality, we speculated that a mouse strain with selective vascular endothelial DDAH1 deficiency (endo-DDAH1(-/-)) would largely abolish tissue DDAH1 expression in many tissues but possibly avoid embryonic lethality. METHODS AND
resultsBy using the LoxP/Cre approach, we generated the endo-DDAH1(-/-) mice. The endo-DDAH1(-/-) mice had no apparent defect in growth or development compared with wild-type littermates. DDAH1 expression was greatly reduced in kidney, lung, brain, and liver, indicating that in these organs DDAH1 is distributed mainly in vascular endothelial cells. The endo-DDAH1(-/-) mice showed a significant increase of asymmetric dimethylarginine concentration in plasma (1.41 micromol/L in the endo-DDAH1(-/-) versus 0.69 micromol/L in the control mice), kidney, lung, and liver, which was associated with significantly increased systolic blood pressure (132 mm Hg versus 113 mm Hg in wild-type). The endo-DDAH1(-/-) mice also exhibited significantly attenuated acetylcholine-induced NO production and vessel relaxation in isolated aortic rings.
conclusionsOur study demonstrates that DDAH1 is highly expressed in vascular endothelium and that endothelial DDAH1 plays an important role in regulating blood pressure. In the context that asymmetric methylarginines are broadly produced by many type of cells, the strong DDAH1 expression in vascular endothelium demonstrates for the first time that vascular endothelium can be an important site to actively dispose of toxic biochemical molecules produced by other types of cells.
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