|
Hypertensive disease
|
0.030 |
GeneticVariation
|
group |
BEFREE |
Both SNP rs805304 and rs2272592 in DDAH2 were not significantly associated with hypertension.
|
22579530 |
2012 |
|
Diabetes Mellitus
|
0.030 |
Biomarker
|
group |
BEFREE |
The purposes of this study were to determine whether suppressed DDAH2 expression would implicate in endothelial dysfunction associated with diabetes mellitus and further to investigate whether adenovirus-mediated DDAH2 gene overexpression could improve the hyperglycemia-induced endothelial dysfunction.
|
19775692 |
2010 |
|
Hypertensive disease
|
0.030 |
GeneticVariation
|
group |
BEFREE |
The present study indicates that the -1151 A/C and -449 G/C polymorphisms in the DDAH2 promoter region are not related to plasma ADMA levels or measures of cardiac structure and function but are associated with an increased prevalence of hypertension.
|
19666123 |
2009 |
|
Cardiovascular Diseases
|
0.030 |
GeneticVariation
|
group |
BEFREE |
The discovery of a functional polymorphism within the DDAH2 promoter suggests that there may be common, individual differences in the ability to metabolise ADMA in vivo, that in turn, might underlie susceptibility to cardiovascular disease.
|
14550280 |
2003 |
|
Diabetes
|
0.020 |
Biomarker
|
disease |
BEFREE |
Considering the involvement of dimethylarginine dimethylaminohydrolase 2 (DDAH2) in diabetes, it was hypothesized that DDAH2 may be beneficial to cardiac function and myocardial fibrosis during the progression of DCM with involvement of the DDAH/asymmetric NG, NGdimethyl‑L‑arginine (ADMA)/nitric oxide synthase (NOS)/nitric oxide (NO) signaling pathway.
|
30569164 |
2019 |
|
Diabetes
|
0.020 |
Biomarker
|
disease |
BEFREE |
Our data demonstrated that inducible nitric oxide synthase/gamma-Glutamyl-cysteine ligase (iNOS/GGCL) and DDAH dysregulation may play a key role in high glucose mediated oxidative stress, whereas HO-1 inducers such as CAPE or its more potent derivatives may be useful in diabetes and other stress-induced pathological conditions.
|
31108850 |
2019 |
|
Myocardial Infarction
|
0.020 |
GeneticVariation
|
disease |
BEFREE |
A functional variant of the dimethylarginine dimethylaminohydrolase-2 gene is associated with myocardial infarction in type 2 diabetic patients.
|
31409409 |
2019 |
|
Septicemia
|
0.020 |
GeneticVariation
|
disease |
BEFREE |
Pilot studies have associated the rs805305 SNP of DDAH2 with ADMA concentrations in sepsis.
|
30538005 |
2018 |
|
Sepsis
|
0.020 |
GeneticVariation
|
disease |
BEFREE |
Pilot studies have associated the rs805305 SNP of DDAH2 with ADMA concentrations in sepsis.
|
30538005 |
2018 |
|
Myocardial Infarction
|
0.020 |
GeneticVariation
|
disease |
BEFREE |
Protective role of DDAH2 (rs805304) gene polymorphism in patients with myocardial infarction.
|
25236572 |
2014 |
|
Septicemia
|
0.020 |
GeneticVariation
|
disease |
BEFREE |
We sought to determine whether functional polymorphisms in DDAH2, which metabolizes the NO synthase inhibitor asymmetric dimethylarginine (ADMA), are associated with susceptibility to sepsis, plasma ADMA, distinct hemodynamic states, and vasopressor requirements in pediatric septic shock.
|
22428028 |
2012 |
|
Sepsis
|
0.020 |
GeneticVariation
|
disease |
BEFREE |
We sought to determine whether functional polymorphisms in DDAH2, which metabolizes the NO synthase inhibitor asymmetric dimethylarginine (ADMA), are associated with susceptibility to sepsis, plasma ADMA, distinct hemodynamic states, and vasopressor requirements in pediatric septic shock.
|
22428028 |
2012 |
|
Kidney Failure, Acute
|
0.010 |
Biomarker
|
disease |
BEFREE |
DDAH-2 alleviates contrast medium iopromide-induced acute kidney injury through nitric oxide synthase.
|
31763675 |
2019 |
|
Erectile dysfunction
|
0.010 |
GeneticVariation
|
disease |
BEFREE |
We aimed to assess whether: 1) ADMA and nitrite levels associated with ED risk and with symptoms intensity; and whether 2) DDAH1 and DDAH2 gene polymorphisms associate with changes in biochemical data, and with ED risk and symptoms intensity.
|
31394201 |
2019 |
|
Diabetic Cardiomyopathies
|
0.010 |
AlteredExpression
|
disease |
BEFREE |
DDAH2 alleviates myocardial fibrosis in diabetic cardiomyopathy through activation of the DDAH/ADMA/NOS/NO pathway in rats.
|
30569164 |
2019 |
|
Sleeplessness
|
0.010 |
Biomarker
|
phenotype |
BEFREE |
Procyanidin B2 from lotus seedpod regulate NO/ADMA/DDAH pathway to treat insomnia in rats.
|
30861604 |
2019 |
|
Cardiomyopathy, Familial Idiopathic
|
0.010 |
Biomarker
|
disease |
BEFREE |
The DCM model rats treated with DDAH2 exhibited reduced left ventricular end‑diastolic pressure, and decreased blood glucose, total cholesterol, triglyceride, fasting blood glucose, and fasting insulin levels, but exhibited increased left ventricular systolic pressure and maximum rate of left ventricular pressure rise/fall levels in myocardial tissues.
|
30569164 |
2019 |
|
Endometritis
|
0.010 |
Biomarker
|
disease |
BEFREE |
The present findings suggest that elevated levels of ADMA are associated with lower DDAH2 and higher PRMT1 in LPS-induced endometritis rat.
|
29119338 |
2018 |
|
Congestive heart failure
|
0.010 |
Biomarker
|
disease |
BEFREE |
Low-dose rosuvastatin exerted cardioprotective effects on isoproterenol-induced heart failure in rats by modulating DDAH-ADMA-NO pathway, and it may present the new therapeutic value in ameliorating chronic heart failure.
|
27957828 |
2017 |
|
Chronic heart failure
|
0.010 |
Biomarker
|
disease |
BEFREE |
Low-dose rosuvastatin exerted cardioprotective effects on isoproterenol-induced heart failure in rats by modulating DDAH-ADMA-NO pathway, and it may present the new therapeutic value in ameliorating chronic heart failure.
|
27957828 |
2017 |
|
Hormone refractory prostate cancer
|
0.010 |
Biomarker
|
disease |
BEFREE |
Here, we discovered a fundamental role of S-phase protein kinase 2 (Skp2) in the formation and progression of CRPC.
|
28346424 |
2017 |
|
Bronchopulmonary Dysplasia
|
0.010 |
Biomarker
|
disease |
BEFREE |
Clinical characteristics and 36 SNPs in DDAH1 and DDAH2 were compared between BPD-associated PH patients (cases) and BPD-alone patients (controls).
|
26663142 |
2016 |
|
Arteriosclerosis
|
0.010 |
PosttranslationalModification
|
disease |
BEFREE |
Homocysteine disrupts EPCs function via inducing the hypermethylation of DDAH2 promoter, suggesting a key role of epigenetic mechanism in the progression of atherosclerosis.
|
24934151 |
2014 |
|
Rheumatoid Arthritis
|
0.010 |
GeneticVariation
|
disease |
BEFREE |
The results of our study give no evidence to suggest that increased ADMA levels in RA relate to DDAH genetic polymorphisms.
|
25194333 |
2014 |
|
Atherosclerosis
|
0.010 |
PosttranslationalModification
|
disease |
BEFREE |
Homocysteine disrupts EPCs function via inducing the hypermethylation of DDAH2 promoter, suggesting a key role of epigenetic mechanism in the progression of atherosclerosis.
|
24934151 |
2014 |