|
Hypercholesterolemia, Familial
|
0.500 |
GeneticVariation
|
disease |
BEFREE |
With the help of genome-wide technology, novel genetic variants have been implicated in CeVD and lipid metabolism such as those in protein convertase subtilisin/kexin type 9 (PCSK9) gene in stroke and familial hypercholesterolemia.
|
26959706 |
2016 |
|
Hyperlipoproteinemia Type IIa
|
0.200 |
GeneticVariation
|
disease |
BEFREE |
With the help of genome-wide technology, novel genetic variants have been implicated in CeVD and lipid metabolism such as those in protein convertase subtilisin/kexin type 9 (PCSK9) gene in stroke and familial hypercholesterolemia.
|
26959706 |
2016 |
|
Cerebrovascular accident
|
0.100 |
GeneticVariation
|
group |
BEFREE |
With the help of genome-wide technology, novel genetic variants have been implicated in CeVD and lipid metabolism such as those in protein convertase subtilisin/kexin type 9 (PCSK9) gene in stroke and familial hypercholesterolemia.
|
26959706 |
2016 |
|
Cerebrovascular Disorders
|
0.010 |
Biomarker
|
group |
BEFREE |
With the help of genome-wide technology, novel genetic variants have been implicated in CeVD and lipid metabolism such as those in protein convertase subtilisin/kexin type 9 (PCSK9) gene in stroke and familial hypercholesterolemia.
|
26959706 |
2016 |
|
Arteriosclerosis
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Wild-type and D374Y-PCSK9 transgenic Yucatan minipigs were fed a high-fat, high-cholesterol diet to induce atherosclerosis and subjected to a clinical FDG-PET and computed tomography scan protocol.
|
31466620 |
2019 |
|
Atherosclerosis
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Wild-type and D374Y-PCSK9 transgenic Yucatan minipigs were fed a high-fat, high-cholesterol diet to induce atherosclerosis and subjected to a clinical FDG-PET and computed tomography scan protocol.
|
31466620 |
2019 |
|
Hyperlipoproteinemia Type IIa
|
0.200 |
Biomarker
|
disease |
BEFREE |
While relatively high cost can be given as a problem, PCSK9 inhibitors are able to reduce LDL cholesterol dramatically even in FH patients who could not achieve targets until now.
|
28784313 |
2018 |
|
Arteriosclerotic cardiovascular disease, NOS
|
0.100 |
Biomarker
|
disease |
BEFREE |
While high-intensity statins remain the first-line treatment to prevent recurrent ASCVD events in secondary prevention patients, ezetimibe and PCSK9 inhibitors are evidence-based non-statin agents that can be used when residual on top of maximally tolerated statin therapy in patients deemed to be at very-high risk of recurrent ASCVD events.
|
30941517 |
2019 |
|
Dyslipidemias
|
0.100 |
GeneticVariation
|
group |
BEFREE |
While gain-of-function mutations aggravate the degradation of LDLR as in familial hypercholesterolemia whereas loss of function mutations reduce the ability of PCSK9 to promote the degradation of LDLR and thus lower the plasma level of LDL-C and dyslipidemia.
|
28450903 |
2017 |
|
Coronary heart disease
|
0.200 |
AlteredExpression
|
disease |
BEFREE |
While exposing the polygenic architecture of circulating lipids and the underpinnings of dyslipidaemia, these genome-wide association studies (GWAS) have provided further evidence of the critical role that lipids play in coronary heart disease (CHD) risk, as indicated by the 2.7-fold enrichment for macrophage gene expression in atherosclerotic plaques and the association of 25 loci (such as PCSK9, APOB, ABCG5-G8, KCNK5, LPL, HMGCR, NPC1L1, CETP, TRIB1, ABO, PMAIP1-MC4R, and LDLR) with CHD.
|
29800275 |
2018 |
|
Dyslipidemias
|
0.100 |
GeneticVariation
|
group |
BEFREE |
While exposing the polygenic architecture of circulating lipids and the underpinnings of dyslipidaemia, these genome-wide association studies (GWAS) have provided further evidence of the critical role that lipids play in coronary heart disease (CHD) risk, as indicated by the 2.7-fold enrichment for macrophage gene expression in atherosclerotic plaques and the association of 25 loci (such as PCSK9, APOB, ABCG5-G8, KCNK5, LPL, HMGCR, NPC1L1, CETP, TRIB1, ABO, PMAIP1-MC4R, and LDLR) with CHD.
|
29800275 |
2018 |
|
Septicemia
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Whether PCSK9 genotype influences long-term outcomes in sepsis survivors is unknown.
|
30473376 |
2018 |
|
Sepsis
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Whether PCSK9 genotype influences long-term outcomes in sepsis survivors is unknown.
|
30473376 |
2018 |
|
Acute Chest Syndrome
|
0.100 |
Biomarker
|
disease |
BEFREE |
Whether PCSK9 mAbs decrease the rates of recurrent cardiovascular events within 3 months following ACS is questionable; however, these agents, unlike statins, may not have pleiotropic benefits on the unstable plaque.
|
23932550 |
2013 |
|
Arteriosclerosis
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Whereas PCSK9 gain-of-function (GOF) mutations are associated with autosomal dominant hypercholesterolemia (ADH) and premature atherosclerosis, PCSK9 loss-of-function (LOF) mutations have a cardio-protective effect and in some cases can lead to familial hypobetalipoproteinemia (FHBL).
|
26586530 |
2016 |
|
Atherosclerosis
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Whereas PCSK9 gain-of-function (GOF) mutations are associated with autosomal dominant hypercholesterolemia (ADH) and premature atherosclerosis, PCSK9 loss-of-function (LOF) mutations have a cardio-protective effect and in some cases can lead to familial hypobetalipoproteinemia (FHBL).
|
26586530 |
2016 |
|
Hyperlipoproteinemia Type IIa
|
0.200 |
GeneticVariation
|
disease |
BEFREE |
Whereas PCSK9 gain-of-function (GOF) mutations are associated with autosomal dominant hypercholesterolemia (ADH) and premature atherosclerosis, PCSK9 loss-of-function (LOF) mutations have a cardio-protective effect and in some cases can lead to familial hypobetalipoproteinemia (FHBL).
|
26586530 |
2016 |
|
Kidney Diseases
|
0.040 |
AlteredExpression
|
group |
BEFREE |
When pooled estimates were derived independently for low- and high-CV risk populations, baseline PCSK9 levels predicted total CV events only in apparently healthy subjects (RR = 1.13, 95% CI: 1.050-1.222, Z = 3.21, p = 0.001) and not in populations with established CV or renal disease (RR = 1.09, 95% CI: 0.961-1.23, Z = 1.33, p = 0.182).
|
27501130 |
2016 |
|
Arteriosclerosis
|
0.100 |
Biomarker
|
disease |
BEFREE |
We tested the therapeutic effect of a PCSK9 vaccine on dyslipidemia and atherosclerosis.
|
31818299 |
2019 |
|
Atherosclerosis
|
0.100 |
Biomarker
|
disease |
BEFREE |
We tested the therapeutic effect of a PCSK9 vaccine on dyslipidemia and atherosclerosis.
|
31818299 |
2019 |
|
Dyslipidemias
|
0.100 |
Biomarker
|
group |
BEFREE |
We tested the therapeutic effect of a PCSK9 vaccine on dyslipidemia and atherosclerosis.
|
31818299 |
2019 |
|
Ischemic stroke
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
We studied whether the PCSK9 gene is linked to the risk of ischemic stroke (IS) and with the development of intracranial atherosclerosis.
|
17940607 |
2007 |
|
Diabetes Mellitus
|
0.100 |
GeneticVariation
|
group |
BEFREE |
We studied the effects of the proprotein convertase subtilisin/kexin type 9 inhibitor evolocumab on fasting plasma glucose, glycated hemoglobin, weight, and new-onset diabetes mellitus.
|
28844508 |
2017 |
|
Diabetes
|
0.100 |
Biomarker
|
disease |
BEFREE |
We sought to investigate the associations of LDL cholesterol-lowering PCSK9 variants with type 2 diabetes and related biomarkers to gauge the likely effects of PCSK9 inhibitors on diabetes risk.
|
27908689 |
2017 |
|
Diabetes Mellitus
|
0.100 |
Biomarker
|
group |
BEFREE |
We sought to investigate the associations of LDL cholesterol-lowering PCSK9 variants with type 2 diabetes and related biomarkers to gauge the likely effects of PCSK9 inhibitors on diabetes risk.
|
27908689 |
2017 |