Hypertensive disease
|
0.700 |
GeneticVariation
|
group |
BEFREE |
It has been reported that the G534A(Glu178/Glu) polymorphism in the HSD11B2 gene is associated with hypertension.
|
22278213 |
2012 |
Hypertensive disease
|
0.700 |
Biomarker
|
group |
BEFREE |
Licorice root, whose active ingredient, glycerrhetinic acid (GA), inhibits renal 11β-HSD2, and thereby causes hypertension in some individuals.
|
28624548 |
2017 |
Hypertensive disease
|
0.700 |
GeneticVariation
|
group |
BEFREE |
Mutations generating inactive enzymes have been described in the HSD11B2 gene in the congenital syndrome of apparent mineralocorticoid excess (AME)--a low renin form of hypertension.
|
9247735 |
1997 |
Hypertensive disease
|
0.700 |
GeneticVariation
|
group |
BEFREE |
Mutations in the HSD11K (HSD11B2) gene encoding this isozyme cause a genetic form of hypertension, the syndrome of apparent mineralocorticoid excess (AME).
|
8865170 |
1996 |
Hypertensive disease
|
0.700 |
GeneticVariation
|
group |
BEFREE |
Mutations in the gene encoding 11beta-HSD2 (HSD11B2) account for an inherited form of hypertension, the syndrome of "Apparent Mineralocorticoid Excess" (AME) where cortisol induces hypertension and hypokalaemia.
|
15134813 |
2004 |
Hypertensive disease
|
0.700 |
GeneticVariation
|
group |
BEFREE |
Mutations in the HSD11B2 gene encoding the kidney (11-HSD2) isozyme of 11beta-hydroxysteroid dehydrogenase cause the syndrome of apparent mineralocorticoid excess, a form of salt-sensitive hypertension.
|
11196453 |
2000 |
Hypertensive disease
|
0.700 |
GeneticVariation
|
group |
BEFREE |
Mutations of the gene encoding 11beta-HSD-2 are responsible for the syndrome of apparent mineralocorticoid excess, in which cortisol illicitly occupies mineralocorticoid receptors, causing hypertension and hypokalaemia.
|
9370341 |
1997 |
Hypertensive disease
|
0.700 |
Biomarker
|
group |
BEFREE |
Our data suggest that HSD11B2 is associated with hypertension in our black subjects with hypertensive end-stage renal disease.
|
8794836 |
1996 |
Hypertensive disease
|
0.700 |
Biomarker
|
group |
BEFREE |
Our data suggest that kidney-specific deficiency of 11β-HSD2 leads to salt-dependent hypertension, which is attributed to mineralocorticoid receptor-epithelial sodium channel-Na<sup>+</sup>-Cl<sup>-</sup> cotransporter activation in the kidney, and provides evidence that renal dysfunction is essential for developing the phenotype of apparent mineralocorticoid excess.
|
28559392 |
2017 |
Hypertensive disease
|
0.700 |
AlteredExpression
|
group |
BEFREE |
Post-translational histone methylation at different histone 3 lysine residues was also observed to control the expression of genes related to AH as lysine-specific demethylase-1(LSD1), HSD11B2, and epithelial sodium channel subunit α (SCNN1A).
|
25035152 |
2015 |
Hypertensive disease
|
0.700 |
Biomarker
|
group |
CTD_human |
Recently, we have studied an unusual patient with mild low-renin hypertension and a homozygous mutation in the HSD11B2 gene.
|
9707624 |
1998 |
Hypertensive disease
|
0.700 |
GeneticVariation
|
group |
BEFREE |
Recently, we have studied an unusual patient with mild low-renin hypertension and a homozygous mutation in the HSD11B2 gene.
|
9707624 |
1998 |
Hypertensive disease
|
0.700 |
Biomarker
|
group |
BEFREE |
Serum F/E ratio and cortisone allow to identify partial 11βHSD2 deficiencies, as occurs in heterozygous subjects, who would be susceptible to develop arterial hypertension.
|
29617893 |
2018 |
Hypertensive disease
|
0.700 |
Biomarker
|
group |
BEFREE |
Statistical analyses using the affected sib-pair method did not show significant linkage between the 11beta-HSD2 microsatellite marker and hypertension.
|
9856363 |
1998 |
Hypertensive disease
|
0.700 |
Biomarker
|
group |
BEFREE |
The hypertension phenotype is also epigenetically modulated by HSD11B2 methylation in subjects heterozygous for the mutation.
|
26126204 |
2015 |
Hypertensive disease
|
0.700 |
GeneticVariation
|
group |
BEFREE |
The aim of the study was to analyze the HSD11B2 gene to assess whether some of its variants might be involved in hypertension.
|
16109323 |
2005 |
Hypertensive disease
|
0.700 |
AlteredExpression
|
group |
BEFREE |
The current study was conducted to determine if reduced 11β-HSD2 activity is also associated with having resistant HTN.
|
28180242 |
2017 |
Hypertensive disease
|
0.700 |
Biomarker
|
group |
BEFREE |
The deactivation of glucocorticoid by 11βHSD2 controls ligand access to glucocorticoid and mineralocorticoid receptors: loss of function promotes salt retention and hypertension.
|
29138984 |
2017 |
Hypertensive disease
|
0.700 |
Biomarker
|
group |
LHGDN |
The decreased activity of 11beta-HSD2 increases the intracellular availability of cortisol, which might be relevant for the pathogenesis of hypertension and preeclampsia.
|
12911547 |
2003 |
Hypertensive disease
|
0.700 |
GeneticVariation
|
group |
BEFREE |
The enhanced cortisol levels are backed by recent genetic findings on HSD11B2 polymorphisms and may promote hypertension.
|
18337758 |
2008 |
Hypertensive disease
|
0.700 |
AlteredExpression
|
group |
BEFREE |
The isozyme 11beta-HSD2 is selectively expressed in mineralocorticoid target tissues and its activity is reduced in various disease states with abnormal sodium retention and hypertension, including the apparent mineralocorticoid excess.
|
25133511 |
2014 |
Hypertensive disease
|
0.700 |
GeneticVariation
|
group |
BEFREE |
The syndrome of AME is a rare form of juvenile hypertension in which 11-HSD is defective.
|
9034789 |
1997 |
Hypertensive disease
|
0.700 |
GeneticVariation
|
group |
BEFREE |
The syndrome of apparent mineralocorticoid excess (AME) is an inherited form of hypertension in which 11 beta-hydroxysteroid dehydrogenase (11 beta-HSD) is defective.
|
8979285 |
1997 |
Hypertensive disease
|
0.700 |
Biomarker
|
group |
CTD_human |
The syndrome of apparent mineralocorticoid excess (AME) is an inherited form of human hypertension thought to result from a deficiency of 11 beta-hydroxysteroid dehydrogenase (11 beta HSD).
|
7670488 |
1995 |
Hypertensive disease
|
0.700 |
Biomarker
|
group |
BEFREE |
The syndrome of apparent mineralocorticoid excess (AME) is an inherited form of human hypertension thought to result from a deficiency of 11 beta-hydroxysteroid dehydrogenase (11 beta HSD).
|
7670488 |
1995 |