Production of free methylarginines via the proteasome and autophagy pathways in cultured cells

Fukamizu, Akiyoshi

doi:10.3892/mmr.2011.488

Cited by 11 publications

(8 citation statements)

References 21 publications

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“…The production of ADMA and L-NMMA is the result of proteolysis of proteins containing methylated arginines (74,81,90). L-NMMA is formed when protein-incorporated L-arginine is methylated by the enzymes protein arginine methyltransferases type I (PRMT-I) or type-II (PRMT-II) (74,81).…”

Section: Adma and L-nmma Production And Removalmentioning

confidence: 99%

Effect of asymmetric dimethylarginine (ADMA) on heart failure development

Liu

Hou

et al. 2016

Nitric Oxide

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Asymmetric dimethylarginine (ADMA) is an endogenous inhibitor of nitric oxide synthases that limits nitric oxide bioavailability and can increase production of NOS derived reactive oxidative species. Increased plasma ADMA is a one of the strongest predictors of mortality in patients who have had a myocardial infarction or suffer from chronic left heart failure, and is also an independent risk factor for several other conditions that contribute to heart failure development, including hypertension, coronary artery disease/atherosclerosis, diabetes, and renal dysfunction. The enzyme responsible for ADMA degradation is dimethylarginine dimethylaminohydrolase-1 (DDAH1). DDAH1 plays an important role in maintaining nitric oxide bioavailability and preserving cardiovascular function in the failing heart. Here, we examine mechanisms of abnormal NO production in heart failure, with particular focus on the role of ADMA and DDAH1.

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Section: Adma and L-nmma Production And Removalmentioning

confidence: 99%

Effect of asymmetric dimethylarginine (ADMA) on heart failure development

Liu

Hou

et al. 2016

Nitric Oxide

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“…While some studies have found decreased ADMA levels in smokers as compared to non-smokers, others have detected increased amounts of ADMA in cigarette smoking subjects [130,131]. Despite conflicting results on arginine metabolism in COPD patients, altered ADMA levels in smokers might be associated with dysregulated PRMT activities and the ubiquitin-proteasome system, an ATP-dependent proteolytic pathway, which has been implicated in the ADMA metabolism [36,37]. …”

Section: Protein Arginine Methyltransferases In Pulmonary Disordersmentioning

confidence: 99%

Protein Arginine Methyltransferases (PRMTs): Promising Targets for the Treatment of Pulmonary Disorders

Zakrzewicz

Preissner

et al. 2012

IJMS

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Protein arginine methylation is a novel posttranslational modification that plays a pivotal role in a variety of intracellular events, such as signal transduction, protein-protein interaction and transcriptional regulation, either by the direct regulation of protein function or by metabolic products originating from protein arginine methylation that influence nitric oxide (NO)-dependent processes. A growing body of evidence suggests that both mechanisms are implicated in cardiovascular and pulmonary diseases. This review will present and discuss recent research on PRMTs and the methylation of non-histone proteins and its consequences for the pathogenesis of various lung disorders, including lung cancer, pulmonary fibrosis, pulmonary hypertension, chronic obstructive pulmonary disease and asthma. This article will also highlight novel directions for possible future investigations to evaluate the functional contribution of arginine methylation in lung homeostasis and disease.

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“…Given that NO has pleiotropic bioactivities, it is not surprising that a variety of important biological functions are regulated by ADMA and SDMA. Emerging clinical and experimental evidence indicates that ADMA and SDMA are involved in the pathophysiology of endothelial dysfunction [13], atherosclerosis [4], oxidative stress [14,15], inflammation [16,17], uremia [8], apoptosis, [18], autophagy [19], and impaired immunological function [20]. …”

Section: Introductionmentioning

confidence: 99%

Toxic Dimethylarginines: Asymmetric Dimethylarginine (ADMA) and Symmetric Dimethylarginine (SDMA)

Tain

Hsu

2017

Toxins

198

195

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Asymmetric and symmetric dimethylarginine (ADMA and SDMA, respectively) are toxic, non-proteinogenic amino acids formed by post-translational modification and are uremic toxins that inhibit nitric oxide (NO) production and play multifunctional roles in many human diseases. Both ADMA and SDMA have emerged as strong predictors of cardiovascular events and death in a range of illnesses. Major progress has been made in research on ADMA-lowering therapies in animal studies; however, further studies are required to fill the translational gap between animal models and clinical trials in order to treat human diseases related to elevated ADMA/SDMA levels. Here, we review the reported impacts of ADMA and SDMA on human health and disease, focusing on the synthesis and metabolism of ADMA and SDMA; the pathophysiological roles of these dimethylarginines; clinical conditions and animal models associated with elevated ADMA and SDMA levels; and potential therapies against ADMA and SDMA. There is currently no specific pharmacological therapy for lowering the levels and counteracting the deleterious effects of ADMA and SDMA. A better understanding of the mechanisms underlying the impact of ADMA and SDMA on a wide range of human diseases is essential to the development of specific therapies against diseases related to ADMA and SDMA.

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Production of free methylarginines via the proteasome and autophagy pathways in cultured cells

Cited by 11 publications

References 21 publications

Effect of asymmetric dimethylarginine (ADMA) on heart failure development

Effect of asymmetric dimethylarginine (ADMA) on heart failure development

Protein Arginine Methyltransferases (PRMTs): Promising Targets for the Treatment of Pulmonary Disorders

Toxic Dimethylarginines: Asymmetric Dimethylarginine (ADMA) and Symmetric Dimethylarginine (SDMA)

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