Article
Cardiac & Cardiovascular Systems
Shiyun Wang, Zixuan Deng, Hong Zhang, Rong Zhang, Dandan Yan, Xiaojiao Zheng, Weiping Jia, Cheng Hu
Summary: Hp genotype affects the association between DDAH 1 rs233109 and diabetic macroangiopathy in Chinese patients with type 2 diabetes.
CARDIOVASCULAR DIABETOLOGY
(2022)
Review
Medicine, General & Internal
Natalia Jarzebska, Ekaterina S. Karetnikova, Alexander G. Markov, Michael Kasper, Roman N. Rodionov, Peter M. Spieth
Summary: Radiation-induced pulmonary fibrosis is a common complication of thoracic tumor radiation therapy, with current therapeutic options being limited to supportive measures like steroids but with unsatisfactory efficacy. Recent studies have shown that lung fibrosis development is a dynamic and complex process involving various cellular and molecular interactions.
FRONTIERS IN MEDICINE
(2021)
Article
Medicine, Research & Experimental
Yichen Zhao, Xiaoye Ma, Yuchen Zhou, Junchao Xie, Xueyuan Liu, Yanxin Zhao
Summary: Dimethylarginine dimethylamino hydrolase-1 (DDAH-1) plays a protective role in ischemic stroke by regulating ADMA levels and preventing tight junction protein degradation, thus protecting the blood-brain barrier. Supplementation of L-arginine helps restore DDAH-1 function.
LABORATORY INVESTIGATION
(2021)
Article
Pharmacology & Pharmacy
Meiting Wu, Ting Li, Ge Li, Bingxuan Niu, Tian Wu, Li Yan, Shiming Wang, Shuangyi He, Chuyi Huang, Weiqiang Tong, Niansheng Li, Junlin Jiang
Summary: This study reveals the underlying mechanisms of ADMA in diabetic cardiomyopathy, specifically focusing on the role of EndMT. It is found that ADMA induces EndMT in cardiac microvascular endothelial cells (HCMECs) under high glucose conditions, while over-expression of DDAH1 protects against EndMT. Additionally, the study identifies the involvement of LncRNA DANCR in the regulation of the FoxO1/DDAH1/ADMA pathway and EndMT. These findings provide new insights into the pathogenesis of diabetic cardiomyopathy and suggest potential therapeutic targets.
EUROPEAN JOURNAL OF PHARMACOLOGY
(2023)
Article
Biochemistry & Molecular Biology
Sakkarai Mohamed Asha Parveen, Sirisha Natani, K. K. Sruthi, Priyanka Khilar, Ramesh Ummanni
Summary: This study found that DDAH1 overexpression in prostate cancer cells is positively regulated by HIF-1 alpha and Nrf2. Under hypoxia, HIF-1 alpha activates DDAH1 expression by binding to the HRE in the promoter region, while in the absence of HIF-1 alpha, Nrf2 promotes DDAH1 expression through AREs.
INTERNATIONAL JOURNAL OF BIOCHEMISTRY & CELL BIOLOGY
(2022)
Article
Cell Biology
Ying Fan, Qiang Gao, Jia-Xin Guan, Lei Liu, Ming Hong, Li Jun, Li Wang, Hai-Feng Ding, Li-Hong Jiang, Bo-Yu Hou, Mei Li, Zhi-Qiang Song, De-Qin Sun, Chao-Qi Yan, Lan Ma
Summary: Cerebrovascular endothelial dysfunction is involved in leukoaraiosis progression. The DDAH2 gene polymorphism is associated with higher plasma asymmetric dimethylarginine levels in patients with leukoaraiosis. GG genotype of DDAH2 (-449 G/C) is more common in patients with leukoaraiosis and is correlated with higher levels of asymmetric dimethylarginine.
NEURAL REGENERATION RESEARCH
(2021)
Article
Biochemistry & Molecular Biology
Sakkarai Mohamed Asha Parveen, Karthik Reddy Kami Reddy, Ramesh Ummanni
Summary: The expression of Dimethylarginine dimethylaminohydrolase-1 (DDAH1) is frequently increased in various cancers, including prostate cancer, and it enhances nitric oxide (NO) production by metabolising endogenous NO synthase (NOS) inhibitors. DDAH1 protects prostate cancer cells from cell death and promotes survival. This study reveals the role of DDAH1 in the antioxidant defense system and its role in promoting cell survival.
NITRIC OXIDE-BIOLOGY AND CHEMISTRY
(2023)
Article
Biochemistry & Molecular Biology
Shan Huang, Zexing Li, Zewen Wu, Chang Liu, Minghang Yu, Mingjie Wen, Liyun Zhang, Xi Wang
Summary: The study reveals that DDAH2 regulates the RLR-mediated antiviral response by inhibiting the MAVS pathway in mitochondria, promoting mitochondrial fission and blocking innate immune responses. TBK1 inhibits DDAH2 through phosphorylation, leading to a reciprocal inhibitory loop between the DDAH2-NO cascade and the RLR signaling pathway.
Review
Pediatrics
Chien-Ning Hsu, You-Lin Tain
Summary: This review summarizes the levels of circulating and urinary ADMA in children and adolescents with kidney disease, as well as its pathophysiological role in the kidneys. Additionally, various analytical methods for measuring ADMA and the issues that need to be addressed before clinical implementation are discussed.
Article
Biochemistry & Molecular Biology
Yukiko K. Kaneko, Ami Morioka, Misaki Sano, Maho Tashiro, Naoya Watanabe, Nahoko Kasahara, Masato Nojiri, Chihiro Ishiwatari, Kentaro Ichinose, Akira Minami, Takashi Suzuki, Momoka Yamaguchi, Toshihide Kimura, Tomohisa Ishikawa
Summary: This study found that high concentrations of glucose and the insulin receptor blocker S661 reduced the expression of DDAH2 in pancreatic β cells, leading to the accumulation of ADMA. The accumulation of ADMA suppressed the production of nitric oxide, resulting in increased apoptosis of pancreatic β cells.
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
(2022)
Article
Multidisciplinary Sciences
Ali Aghdassi, Edzard Schwedhelm, Dorothee Atzler, Matthias Nauck, Jens-Peter Kuehn, Marie-Luise Kromrey, Henry Voelzke, Stephan B. Felix, Marcus Doerr, Till Ittermann, Martin Bahls
Summary: Homoarginine (hArg), a non-essential amino acid, inhibits hepatic alkaline phosphatases and affects bile secretion. In this study, we investigated the relationship between hArg and liver biomarkers and evaluated the impact of hArg supplementation. Our results showed that hArg was positively associated with ALT, AST, GGT, AP, albumin, total bilirubin, cholinesterase, Quick's value, liver fat, and MELD score. However, hArg supplementation did not affect liver biomarkers. These findings suggest that hArg may serve as a marker of liver dysfunction and warrant further exploration.
SCIENTIFIC REPORTS
(2023)
Article
Cardiac & Cardiovascular Systems
Carolina Averta, Elettra Mancuso, Rosangela Spiga, Sofia Miceli, Elena Succurro, Teresa Vanessa Fiorentino, Maria Perticone, Gaia Chiara Mannino, Prapaporn Jungtrakoon Thamtarana, Angela Sciacqua, Giorgio Sesti, Francesco Andreozzi
Summary: This study found that individuals carrying the rs9267551 C allele in the DDAH2 gene had lower carotid-femoral pulse wave velocity (cfPWV), suggesting reduced arterial stiffness. Further analysis revealed that the variation in ADMA levels mediated the effect of the DDAH2 rs9267551 genotype on cfPWV.
FRONTIERS IN CARDIOVASCULAR MEDICINE
(2022)
Article
Biochemistry & Molecular Biology
Arduino A. Mangoni, Tommaso Ceruti, Roberta Frapolli, Massimo Russo, Stefania Fichera, Massimo Zucchetti, Sara Tommasi
Summary: This study investigated the pharmacokinetic profile of ZST316 and ZST152, arginine analogues with inhibitory activity towards DDAH1, in mice. The results showed that ZST316 has a favorable pharmacokinetic profile and can be used to study the effects of DDAH1 inhibition through intraperitoneal administration.
Article
Endocrinology & Metabolism
Tien F. Lee, Sara Tommasi, Andrew Bersten, Leonie K. Heilbronn, Salvatore Sotgia, Angelo Zinellu, Ciriaco Carru, Arduino A. Mangoni, Morton G. Burt
Summary: This study aimed to investigate whether hyperglycemia may link to mortality in ICU patients through changes in arginine metabolite concentrations. The results showed that plasma ADMA was not significantly associated with any measure of hyperglycemia. L-homoarginine was positively associated with glucose and SHR, but as it is a negative predictor of mortality, the direction of these associations are the opposite of those expected. In vitro DDAH1 activity was not significantly influenced by glucose concentrations. Therefore, the association between relative hyperglycemia and mortality in critically ill patients is not mediated by changes in ADMA or L-homoarginine.
DIABETOLOGY & METABOLIC SYNDROME
(2023)
Article
Cardiac & Cardiovascular Systems
Irakli Kopaliani, Natalia Jarzebska, Silke Billoff, Anne Kolouschek, Jens Martens-Lobenhoffer, Stefan R. Bornstein, Stefanie M. Bode-Boeger, Vinitha N. Ragavan, Norbert Weiss, Arduino A. Mangoni, Andreas Deussen, Roman N. Rodionov
Summary: In this study, overexpression of dimethylarginine dimethylaminohydrolase 1 (DDAH1) was found to protect against angiotensin II-induced cardiovascular damage, progression of hypertension, and adverse vascular remodeling in vivo. This protective effect is associated with decreased levels of asymmetric dimethylarginine, preservation of endothelial function, inhibition of cardiovascular inflammation, and lower activity of matrix metalloproteinase-2. The findings suggest that upregulation of DDAH1 might be a promising therapeutic approach against angiotensin II-induced end organ damage.
AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY
(2021)
