Acute myocardial infarction
|
0.010 |
Biomarker
|
disease |
BEFREE |
Herein, we used an inducible cardiac-specific DDAH1 knockdown mouse (cardiac DDAH1<sup>-/-</sup>) to investigate the role of cardiomyocyte DDAH1 in left-ventricular (LV) remodeling after acute myocardial infarction (AMI).
|
29892894 |
2018 |
Adenocarcinoma of lung (disorder)
|
0.010 |
Biomarker
|
disease |
BEFREE |
Overall, our data revealed that long non-coding RNA H19 confers resistance to gefitinib via miR-148b/dimethylarginine dimethylaminohydrolase-1 axis in lung adenocarcinoma, which offers a new insight into the epidermal growth factor receptor tyrosine kinase inhibitors therapy resistance.
|
31503013 |
2020 |
Alzheimer's Disease
|
0.010 |
AlteredExpression
|
disease |
BEFREE |
Our findings suggest that strategies to increase DDAH1 activity in neuronal cells may be a novel approach to attenuating AD development.
|
25499850 |
2015 |
Amyloidosis
|
0.010 |
AlteredExpression
|
disease |
BEFREE |
However, overexpression of dimethylarginine dimethylaminohydrolase 1 (DDAH1) to promote ADMA degradation significantly attenuated oxidative stress and Aβ secretion in APPsw cells.
|
25499850 |
2015 |
Arteriosclerosis
|
0.010 |
Biomarker
|
disease |
BEFREE |
In human subjects (n = 89) the FoxO1/DDAH1/ADMA pathway marks unstable atherosclerosis.
|
26226438 |
2015 |
Atherosclerosis
|
0.010 |
Biomarker
|
disease |
BEFREE |
In human subjects (n = 89) the FoxO1/DDAH1/ADMA pathway marks unstable atherosclerosis.
|
26226438 |
2015 |
Body Height
|
0.100 |
GeneticVariation
|
phenotype |
GWASCAT |
Leveraging Polygenic Functional Enrichment to Improve GWAS Power.
|
30595370 |
2019 |
Body Height
|
0.100 |
GeneticVariation
|
phenotype |
GWASCAT |
Characterizing rare and low-frequency height-associated variants in the Japanese population.
|
31562340 |
2019 |
Body mass index
|
0.100 |
GeneticVariation
|
phenotype |
GWASCAT |
Leveraging Polygenic Functional Enrichment to Improve GWAS Power.
|
30595370 |
2019 |
Breast Carcinoma
|
0.020 |
Biomarker
|
disease |
BEFREE |
This study represents the first evidence for therapeutic inhibition of DDAH1 by small molecules in breast cancer.
|
30611984 |
2019 |
Breast Carcinoma
|
0.020 |
AlteredExpression
|
disease |
BEFREE |
Here, we identified over-expression of DDAH1 in aggressive MDA-MB-231, MDA-MB-453 and BT549 breast cancer cell lines when compared to normal mammary epithelial cells.
|
29070803 |
2017 |
Bronchopulmonary Dysplasia
|
0.010 |
GeneticVariation
|
disease |
BEFREE |
The rs480414 SNP in DDAH1 may be protective against the development of PH in patients with BPD.
|
26663142 |
2016 |
Cardiomyopathy, Familial Idiopathic
|
0.010 |
Biomarker
|
disease |
BEFREE |
To further investigate the underlying regulatory mechanism of DDAH2 in DCM, the contents of ADMA and NO, and the activities of DDAH and NOS were observed.
|
30569164 |
2019 |
Cardiovascular Diseases
|
0.020 |
Biomarker
|
group |
BEFREE |
This study comprised a genome-wide association analysis of 3 well-characterized population-based cohorts (Framingham Heart Study [FHS; n=2992], Gutenberg Health Study [GHS; n=4354], and Multinational Monitoring of Trends and Determinants in Cardiovascular Disease Study [MONICA]/Cooperative Health Research in the Augsburg Area, Augsburg, Bavaria, Germany [KORA] F3 [n=581]) and identified replicated loci (DDAH1, MED23, Arg1, and AGXT2) associated with the interindividual variability in ADMA, l-arginine, and SDMA.
|
25245031 |
2014 |
Cardiovascular Diseases
|
0.020 |
GeneticVariation
|
group |
BEFREE |
In that study a novel functional mutation of DDAH-1 was identified; the mutation carriers had a significantly elevated risk for cardiovascular disease and a tendency to develop hypertension.
|
16444868 |
2005 |
Carotid Artery Thrombosis
|
0.010 |
Biomarker
|
disease |
BEFREE |
DDAH1 Tg mice also were protected from hypertrophy of cerebral arterioles (P<0.05) but not from accelerated carotid artery thrombosis induced by the HM/LF diet.
|
20019334 |
2010 |
Central post-stroke pain
|
0.010 |
AlteredExpression
|
phenotype |
BEFREE |
These results suggest that mechanical allodynia in the early stage of CPSP is caused by increment of NOS activity through upregulated DDAH1 in the spinal cord.
|
31474717 |
2019 |
Cerebrovascular accident
|
0.010 |
GeneticVariation
|
group |
BEFREE |
Our results suggest that the DDAH1 loss-of-function polymorphism is associated with both increased risk of thrombosis stroke and CHD.
|
20167924 |
2010 |
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 |
Chronic Kidney Diseases
|
0.020 |
AlteredExpression
|
group |
BEFREE |
Emerging evidence suggests that plasma ADMA accumulation and DDAH1 activity/expression reduction are linked to chronic kidney disease (CKD) pathology, but the mechanisms remain largely unknown.
|
28594240 |
2017 |
Chronic Kidney Diseases
|
0.020 |
GeneticVariation
|
group |
BEFREE |
We conclude that polymorphisms in DDAH1 alter the rate of decline of glomerular filtration rate in subjects with chronic kidney disease.
|
20010544 |
2010 |
Cirrhosis
|
0.010 |
Biomarker
|
disease |
BEFREE |
DDAH-1 immunohistochemistry was conducted on human cirrhosis and healthy liver tissue.
|
25152204 |
2015 |
Congestive heart failure
|
0.020 |
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 |
Congestive heart failure
|
0.020 |
Biomarker
|
disease |
BEFREE |
Here, we examine mechanisms of abnormal NO production in heart failure, with particular focus on the role of ADMA and DDAH1.
|
26923818 |
2016 |
Coronary Arteriosclerosis
|
0.020 |
GeneticVariation
|
disease |
BEFREE |
A novel loss-of-function DDAH1 promoter polymorphism is associated with increased susceptibility to thrombosis stroke and coronary heart disease.
|
20167924 |
2010 |