|
Cardiovascular Diseases
|
0.200 |
GeneticVariation
|
group |
LHGDN |
The D374Y gain-of-function mutant, associated with hypercholesterolemia and early-onset cardiovascular disease, binds the receptor 25 times more tightly than wild-type PCSK9 at neutral pH and remains exclusively in a high-affinity complex at the acidic pH.
|
17435765 |
2007 |
|
Cardiovascular Diseases
|
0.200 |
GeneticVariation
|
group |
BEFREE |
The D374Y gain-of-function mutant, associated with hypercholesterolemia and early-onset cardiovascular disease, binds the receptor 25 times more tightly than wild-type PCSK9 at neutral pH and remains exclusively in a high-affinity complex at the acidic pH.
|
17435765 |
2007 |
|
Cardiovascular Diseases
|
0.200 |
Biomarker
|
group |
BEFREE |
The proprotein convertase PCSK9 gene is the third locus implicated in familial hypercholesterolemia, emphasizing its role in cardiovascular diseases.
|
18039658 |
2008 |
|
Cardiovascular Diseases
|
0.200 |
GeneticVariation
|
group |
BEFREE |
Our data support the concept that the rare allele of the R46L SNP at the PCSK9 locus significantly lowers LDL C, but does not greatly reduce CHD risk in an elderly population with a high prevalence of cardiovascular disease.
|
18262190 |
2008 |
|
Cardiovascular Diseases
|
0.200 |
Biomarker
|
group |
BEFREE |
Our study indicates that the serum PCSK9 level may be a biomarker of metabolic status and cardiovascular disease.
|
21040917 |
2010 |
|
Cardiovascular Diseases
|
0.200 |
Biomarker
|
group |
BEFREE |
PCSK9 inhibition represents a very promising target for reducing LDL-C levels and decreasing the risk of atherosclerotic cardiovascular diseases, but human clinical trials will be crucial to assess the potency and safety of PCSK9 inhibitors.
|
21619378 |
2011 |
|
Cardiovascular Diseases
|
0.200 |
AlteredExpression
|
group |
BEFREE |
Increased level of PCSK9 functional activity will lead to an accumulation of cholesterol in the blood - a high risk factor for cardiovascular disease.
|
22519528 |
2012 |
|
Cardiovascular Diseases
|
0.200 |
Biomarker
|
group |
BEFREE |
Proprotein convertase subtilisin/kexin type 9 (PCSK9) has emerged as a novel target for controlling plasma levels of low-density lipoprotein cholesterol (LDL-C) and decreasing the risk of cardiovascular diseases.
|
22311433 |
2012 |
|
Cardiovascular Diseases
|
0.200 |
Biomarker
|
group |
BEFREE |
Initial data from investigations of PCSK9 inhibition in humans are promising and indicate that PCSK9 inhibition may be a viable new therapeutic option for the treatment of dyslipidemia and associated cardiovascular diseases.
|
22811413 |
2012 |
|
Cardiovascular Diseases
|
0.200 |
Biomarker
|
group |
BEFREE |
Current research and clinical trial results indicate that a PCSK9 inhibitor may be an exciting new therapeutic drug for the treatment of dyslipidemia and relevant cardiovascular diseases.
|
23578522 |
2013 |
|
Cardiovascular Diseases
|
0.200 |
Biomarker
|
group |
BEFREE |
A decade after our discovery of the involvement of proprotein convertase subtilisin/kexin type 9 (PCSK9) in cholesterol metabolism through the identification of the first mutations leading to hypercholesterolemia, PCSK9 has become one of the most promising targets in cholesterol and cardiovascular diseases.
|
25052769 |
2014 |
|
Cardiovascular Diseases
|
0.200 |
GeneticVariation
|
group |
BEFREE |
Rare gain-of-function PCSK9 variants lead to higher levels of LDL-cholesterol and increased risk of cardiovascular disease; more common loss-of-function PCSK9 variants are associated with reductions in both LDL-cholesterol and risk of cardiovascular disease.
|
24625727 |
2014 |
|
Cardiovascular Diseases
|
0.200 |
GeneticVariation
|
group |
BEFREE |
PCSK9 R46L, lower LDL, and cardiovascular disease risk in familial hypercholesterolemia: a cross-sectional cohort study.
|
25278291 |
2014 |
|
Cardiovascular Diseases
|
0.200 |
AlteredExpression
|
group |
BEFREE |
In contrast, humans with high levels of PCSK9 have higher level of plasma LDL-C and significantly enhanced CVD risk during their lifetime, gain-of-function mutations on PCSK9 are, for instance, causatively associated with familial hypercholesterolaemia (FH).
|
25856746 |
2015 |
|
Cardiovascular Diseases
|
0.200 |
AlteredExpression
|
group |
BEFREE |
Homozygous autosomal dominant hypercholesterolaemia (hoADH), an orphan disease caused by mutations in low-density lipoprotein receptor (LDLR), apolipoprotein B (APOB), or proprotein convertase subtilisin-kexin type 9 (PCSK9), is characterized by elevated plasma low-density lipoprotein-cholesterol (LDL-C) levels and high risk for premature cardiovascular disease (CVD).
|
24585268 |
2015 |
|
Cardiovascular Diseases
|
0.200 |
GeneticVariation
|
group |
BEFREE |
Both OLR1 and PCSK9 genes are associated with atherosclerosis, cardiovascular disease and ischemic stroke.
|
26666837 |
2015 |
|
Cardiovascular Diseases
|
0.200 |
GeneticVariation
|
group |
BEFREE |
PCSK9 GOF mutation carriers have elevated LDL-C levels and are at high risk of premature cardiovascular disease.
|
26374825 |
2015 |
|
Cardiovascular Diseases
|
0.200 |
Biomarker
|
group |
BEFREE |
The development of therapeutic approaches that inhibit PCSK9 function has therefore attracted considerable attention from clinicians and the pharmaceutical industry for the management of hypercholesterolemia and its associated cardiovascular disease risk.
|
26503748 |
2015 |
|
Cardiovascular Diseases
|
0.200 |
Biomarker
|
group |
BEFREE |
Over the last decade, inhibition of Proprotein Convertase Subtilisin/Kexin type 9 (PCSK9) has emerged as a promising target to reduce residual cardiovascular disease risk.
|
25989132 |
2015 |
|
Cardiovascular Diseases
|
0.200 |
Biomarker
|
group |
BEFREE |
Pharmacologic inhibitors of proprotein convertase subtilisin-kexin type 9 (PCSK9) are being evaluated in clinical trials for the treatment of cardiovascular disease.
|
27959767 |
2016 |
|
Cardiovascular Diseases
|
0.200 |
GeneticVariation
|
group |
BEFREE |
The new treatment strategies for lipid-lowering therapy include using proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitors as an exciting approach to reduce residual risk of cardiovascular diseases (CVD).
|
27865998 |
2017 |
|
Cardiovascular Diseases
|
0.200 |
GeneticVariation
|
group |
BEFREE |
Autosomal dominant hypercholesterolemia (ADH), characterized by high-plasma low-density lipoprotein cholesterol (LDL-C) levels and premature cardiovascular disease (CVD) risk, is caused by mutations in LDLR, APOB, and/or PCSK9.
|
27919364 |
2017 |
|
Cardiovascular Diseases
|
0.200 |
Biomarker
|
group |
BEFREE |
Mechanisms for modulation of those targets are also becoming more diverse while statins remain the backbone of CVD prevention, the new alternatives, such as PCSK9 monoclonals will probably play an important additional role in treatment of patients at risk for CVD.
|
28445176 |
2017 |
|
Cardiovascular Diseases
|
0.200 |
GeneticVariation
|
group |
BEFREE |
In the entire cohort, the third vs first tertile of PCSK9 was not associated with the risk of death from any cause (hazard ratio = 1.09, p = 0.367) and from cardiovascular diseases (hazard ratio = 1.09, p = 0.476).
|
28436724 |
2017 |
|
Cardiovascular Diseases
|
0.200 |
AlteredExpression
|
group |
BEFREE |
The aim of this review is to outline current findings on the metabolic and dietary regulation of PCSK9 and effects on cholesterol, apoB lipoprotein metabolism, and cardiovascular disease (CVD) risk.
|
28179493 |
2017 |