Heart failure
|
0.600 |
Biomarker
|
disease |
BEFREE |
Atrial and brain natriuretic peptides (ANP and BNP) are established diagnostic and prognostic markers in heart failure, but their utility in patients with advanced cancer is unclear.
|
31128228 |
2019 |
Congestive heart failure
|
0.600 |
Biomarker
|
disease |
BEFREE |
Atrial and brain natriuretic peptides (ANP and BNP) are established diagnostic and prognostic markers in heart failure, but their utility in patients with advanced cancer is unclear.
|
31128228 |
2019 |
Hypertensive disease
|
0.600 |
GeneticVariation
|
group |
BEFREE |
The findings suggested that a common NPPA SNPs rs5063 was associated with serum ANP levels and ANP was prospectively associated with hypertension in the Chinese Han population.
|
31341238 |
2019 |
Hypertensive disease
|
0.600 |
Biomarker
|
group |
BEFREE |
The natriuretic peptide (NP) family (including ANP (atrial natriuretic peptide), BNP (brain natriuretic peptide), and CNP (C-type natriuretic peptide)), the NP receptors (NPRA, NPRB, and NPRC), and the related protease convertases (furin, corin, and PCSK6) constitute the NP system and represent relevant protective mechanisms toward the development of hypertension and associated conditions, such as atherosclerosis, stroke, myocardial infarction, heart failure, and renal injury.
|
30781751 |
2019 |
Heart failure
|
0.600 |
Biomarker
|
disease |
BEFREE |
In contrast, levels of neprilysin (p<0.01), cGMP (p<0.001), and ANP (p<0.001) were higher in systolic dysfunction patients than controls and were the highest in patients with dHF.
|
30148170 |
2018 |
Heart failure
|
0.600 |
Biomarker
|
disease |
BEFREE |
Functionally, knockdown of BRD4 greatly downregulated the NPPA and NPPB in vivo and in vitro, improved the hemodynamic and biometric parameters in rat with heart failure, as well as decreased the apoptosis occurrence.
|
29352508 |
2018 |
Congestive heart failure
|
0.600 |
Biomarker
|
disease |
BEFREE |
Functionally, knockdown of BRD4 greatly downregulated the NPPA and NPPB in vivo and in vitro, improved the hemodynamic and biometric parameters in rat with heart failure, as well as decreased the apoptosis occurrence.
|
29352508 |
2018 |
Congestive heart failure
|
0.600 |
Biomarker
|
disease |
BEFREE |
In contrast, levels of neprilysin (p<0.01), cGMP (p<0.001), and ANP (p<0.001) were higher in systolic dysfunction patients than controls and were the highest in patients with dHF.
|
30148170 |
2018 |
Heart failure
|
0.600 |
AlteredExpression
|
disease |
BEFREE |
In mice with PPCM due to a cardiomyocyte-specific knockout of STAT3 (CKO) neither low nor high dose of recombinant Relaxin-2 (serelaxin, sRlx-LD: 30 µg/kg/day; sRlx-HD: 300 µg/kg/day) affected cardiac fibrosis, inflammation and heart failure but sRlx-HD increased capillary/cardiomyocyte ratio. sRlx-HD significantly increased heart/body weight ratio and cardiomyocyte cross-sectional area in postpartum CKO and wild-type mice without changing the foetal gene expression program (ANP or β-MHC). sRlx-HD augmented plasma Prolactin levels in both genotypes, which induced cardiac activation of STAT5.
|
28453725 |
2017 |
Congestive heart failure
|
0.600 |
AlteredExpression
|
disease |
BEFREE |
In mice with PPCM due to a cardiomyocyte-specific knockout of STAT3 (CKO) neither low nor high dose of recombinant Relaxin-2 (serelaxin, sRlx-LD: 30 µg/kg/day; sRlx-HD: 300 µg/kg/day) affected cardiac fibrosis, inflammation and heart failure but sRlx-HD increased capillary/cardiomyocyte ratio. sRlx-HD significantly increased heart/body weight ratio and cardiomyocyte cross-sectional area in postpartum CKO and wild-type mice without changing the foetal gene expression program (ANP or β-MHC). sRlx-HD augmented plasma Prolactin levels in both genotypes, which induced cardiac activation of STAT5.
|
28453725 |
2017 |
Hypertensive disease
|
0.600 |
GeneticVariation
|
group |
BEFREE |
This study examined the SNPs AGT rs699 (Met235Thr), ADD1 rs4961 (rs4961" genes_norm="118">Gly460Trp), NPPA rs5063 (Val32Met), GPX1 rs1050450 (Pro198Leu), and AGTR1 rs5186 (A1166C) in relation to hypertension and salt sensitivity.
|
27480094 |
2017 |
Hypertensive disease
|
0.600 |
GeneticVariation
|
group |
BEFREE |
In whites, the minor G allele of the atrial natriuretic peptide (ANP) genetic variant rs5068 is associated with higher circulating levels of ANP and B-type natriuretic peptide (BNP), lower risk of hypertension, higher high-density lipoprotein (HDL) cholesterol plasma levels, and lower prevalence of obesity and metabolic syndrome.
|
29253899 |
2017 |
Hypertensive disease
|
0.600 |
GeneticVariation
|
group |
BEFREE |
As a risk factor, ANP gene polymorphisms may affect hypertension.
|
27413750 |
2016 |
Hypertensive disease
|
0.600 |
GeneticVariation
|
group |
BEFREE |
Variants in the human NPPA gene, encoding the ANP precursor, are associated with hypertension, stroke, coronary artery disease, heart failure (HF) and obesity.
|
26074089 |
2015 |
Heart failure
|
0.600 |
Biomarker
|
disease |
BEFREE |
The atrium is the major site of ANP synthesis, which has been said to increase in heart failure as a result of increased production in the left ventricular (LV) myocardium.
|
24599027 |
2014 |
Heart failure
|
0.600 |
GeneticVariation
|
disease |
BEFREE |
Up-regulation was evident for muscle LIM protein (Mlp), desmin, and heart failure (natriuretic peptide A [Nppa], Nppb, and myosin heavy chain 6) and fibrosis (transforming growth factor beta 1, alpha-smooth muscle actin, osteopontin, and periostin) markers.
|
25541130 |
2014 |
Congestive heart failure
|
0.600 |
Biomarker
|
disease |
BEFREE |
The atrium is the major site of ANP synthesis, which has been said to increase in heart failure as a result of increased production in the left ventricular (LV) myocardium.
|
24599027 |
2014 |
Congestive heart failure
|
0.600 |
GeneticVariation
|
disease |
BEFREE |
Up-regulation was evident for muscle LIM protein (Mlp), desmin, and heart failure (natriuretic peptide A [Nppa], Nppb, and myosin heavy chain 6) and fibrosis (transforming growth factor beta 1, alpha-smooth muscle actin, osteopontin, and periostin) markers.
|
25541130 |
2014 |
Hypertensive disease
|
0.600 |
GeneticVariation
|
group |
BEFREE |
Among others, the 2238T>C exon 3 variant has been associated with endothelial cell damage and dysfunction and with an increased risk of acute cardiovascular events, a frameshift mutation within exon 3 has been related to increased risk of atrial fibrillation, and ANP gene variants have been linked to increased risk of hypertension in different ethnic groups.
|
24611929 |
2014 |
Heart failure
|
0.600 |
Therapeutic
|
disease |
RGD |
Histone deacetylase inhibition improved cardiac functions with direct antifibrotic activity in heart failure.
|
23931972 |
2013 |
Heart failure
|
0.600 |
Biomarker
|
disease |
BEFREE |
In experimental early stage HF characterized with marked atrial fibrosis, ANP, BNP, and CNP mRNA, and protein concentrations were higher in HF LA but not HF LV compared with normals.
|
23152112 |
2013 |
Congestive heart failure
|
0.600 |
Therapeutic
|
disease |
RGD |
Histone deacetylase inhibition improved cardiac functions with direct antifibrotic activity in heart failure.
|
23931972 |
2013 |
Congestive heart failure
|
0.600 |
Biomarker
|
disease |
BEFREE |
In experimental early stage HF characterized with marked atrial fibrosis, ANP, BNP, and CNP mRNA, and protein concentrations were higher in HF LA but not HF LV compared with normals.
|
23152112 |
2013 |
Hypertensive disease
|
0.600 |
Biomarker
|
group |
CTD_human |
Quercetin inhibits left ventricular hypertrophy in spontaneously hypertensive rats and inhibits angiotensin II-induced H9C2 cells hypertrophy by enhancing PPAR-γ expression and suppressing AP-1 activity.
|
24039778 |
2013 |
Hypertensive disease
|
0.600 |
Therapeutic
|
group |
CTD_human |
Quercetin inhibits left ventricular hypertrophy in spontaneously hypertensive rats and inhibits angiotensin II-induced H9C2 cells hypertrophy by enhancing PPAR-γ expression and suppressing AP-1 activity.
|
24039778 |
2013 |