A5025125672- Nitric Oxide and Endothelin Effects
- Adenosine and Purinergic Signaling
- Amino Acid Enzymes and Metabolism
- Renin-Angiotensin System Studies
- Cancer-related gene regulation
- Neuroendocrine regulation and behavior
- Tissue Engineering and Regenerative Medicine
- Epigenetics and DNA Methylation
- Peroxisome Proliferator-Activated Receptors
- Neurotransmitter Receptor Influence on Behavior
- Tryptophan and brain disorders
- Cardiovascular Issues in Pregnancy
Technische Universität Dresden
2021-2023
University Hospital Carl Gustav Carus
2021
Flinders Medical Centre
2021
Flinders University
2021
Abstract Dimethylarginine dimethylaminohydrolase 1 (DDAH1) protects against cardiovascular disease by metabolising the risk factor asymmetric dimethylarginine (ADMA). However, question whether second DDAH isoform, DDAH2, directly metabolises ADMA has remained unanswered. Consequently, it is still unclear if DDAH2 may be a potential target for ADMA-lowering therapies or drug development efforts should focus on DDAH2’s known physiological functions in mitochondrial fission, angiogenesis,...
Abstract The endogenous methylated derivative of ʟ-arginine, N ω , ′ -dimethyl-ʟ-arginine (asymmetric dimethylarginine, ADMA), an independent risk factor in many diseases, inhibits the activity nitric oxide synthases and, consequently, modulates availability oxide. While most studies on biological role ADMA have focused endothelial and inducible modulation its contribution to cardiovascular, metabolic, renal a regulating neuronal pathologies central nervous system is less understood. two...
The enzyme dimethylarginine dimethylaminohydrolase 1 (DDAH1) plays a pivotal role in the regulation of nitric oxide levels by degrading main endogenous synthase inhibitor asymmetric (ADMA). Growing evidence highlight potential implication DDAH/ADMA axis etiopathogenesis several neuropsychiatric and neurological disorders, yet underlying molecular mechanisms remain elusive. In this study, we sought to investigate DDAH1 behavioral endophenotypes with relevance. To achieve this, global...
We showed that overexpression of dimethylarginine dimethylaminohydrolase 1 (DDAH1) protects from angiotensin II-induced cardiovascular damage, progression hypertension, and adverse vascular remodeling in vivo. This protective effect strongly depends on the dose duration II infusion is associated with decreased levels asymmetric (ADMA), preservation endothelial function, inhibition inflammation, as well lower activity matrix metalloproteinase-2 (MMP2). Our findings are highly clinically...
Abstract The endogenous methylated derivative of L-arginine, N G -N -dimethyl-ʟ-arginine (asymmetric dimethylarginine, ADMA), an independent risk factor in many diseases, inhibits the activity nitric oxide synthases and, consequently, modulates availability oxide. While most studies on biological role ADMA have focused endothelial and inducible modulation its contribution to cardiovascular, metabolic, renal a regulating neuronal pathologies central nervous system is less understood. two...
Abstract The endogenous methylated derivative of L-arginine, N G -N -dimethyl-ʟ-arginine (asymmetric dimethylarginine, ADMA), an independent risk factor in many diseases, inhibits the activity nitric oxide synthases and, consequently, modulates availability oxide. While most studies on biological role ADMA have focused endothelial and inducible modulation its contribution to cardiovascular, metabolic, renal a regulating neuronal pathologies central nervous system is less understood. two...