|
Hypercholesterolemia
|
0.700 |
Biomarker
|
disease |
BEFREE |
Effect of PCSK9 Inhibitors on Clinical Outcomes in Patients With Hypercholesterolemia: A Meta-Analysis of 35 Randomized Controlled Trials.
|
29223954 |
2017 |
|
Hypercholesterolemia
|
0.700 |
Biomarker
|
disease |
BEFREE |
Three genes causative for FH (LDLR, APOB, and PCSK9) were sequenced in 636 patients with severe hypercholesterolaemia (mean age, 45 years; 300 males [47%], CAD diagnosis, 185 [29%]), and the presence of clinical FH signs (xanthoma and/or family history) were assessed.
|
28159968 |
2017 |
|
Hypercholesterolemia
|
0.700 |
Biomarker
|
disease |
BEFREE |
Potential role of lycopene in targeting proprotein convertase subtilisin/kexin type-9 to combat hypercholesterolemia.
|
28412198 |
2017 |
|
Hypercholesterolemia
|
0.700 |
Biomarker
|
disease |
BEFREE |
The effects of PCSK9 on the LDL receptor, the relationship of this convertase with IDOL, and treatments currently available against hypercholesterolemia are also discussed.
|
28587771 |
2017 |
|
Hypercholesterolemia
|
0.700 |
AlteredExpression
|
disease |
BEFREE |
In conclusion, maternal hypercholesterolemia might decrease the transportation of cholesterol from mother to fetus because of the high levels of PCSK9 protein expression.
|
28199412 |
2017 |
|
Hypercholesterolemia
|
0.700 |
Biomarker
|
disease |
BEFREE |
Proprotein convertase subtilisin/kexin type 9 (PCSK9) has emerged as a promising therapeutic target for the treatment of hypercholesterolaemia and atherosclerosis.
|
28637178 |
2017 |
|
Hypercholesterolemia
|
0.700 |
Biomarker
|
disease |
BEFREE |
Proprotein convertase subtilisin/kexin type 9 (PCSK9) impedes low‑density lipoprotein (LDL) receptor (LDLR)-mediated LDL-cholesterol uptake and has hence emerged as a critical regulator of serum cholesterol levels and a new therapeutic target for the treatment of hypercholesterolemia.
|
28204827 |
2017 |
|
Hypercholesterolemia
|
0.700 |
Biomarker
|
disease |
BEFREE |
To gain insight into recruitment of different plaque SMCs, we mapped their clonal architecture in aggregation chimeras of eGFP+Apoe-/- and Apoe-/- mouse embryos and in mice with a mosaic expression of fluorescent proteins in medial SMCs that were rendered atherosclerotic by PCSK9-induced hypercholesterolemia.
|
28978793 |
2017 |
|
Hypercholesterolemia
|
0.700 |
Biomarker
|
disease |
BEFREE |
For example, silencing messenger RNA (mRNA of PCSK9) is a new alternative against hypercholesterolemia.
|
29209441 |
2017 |
|
Hypercholesterolemia
|
0.700 |
Biomarker
|
disease |
BEFREE |
PCSK9 Inhibition With Monoclonal Antibodies: Modern Management of Hypercholesterolemia.
|
27195910 |
2017 |
|
Hypercholesterolemia
|
0.700 |
Biomarker
|
disease |
BEFREE |
PCSK9 (proprotein convertase subtilisin/kexin type 9) inhibitors have emerged as the add-on therapy on top of statins and/or ezetimibe for the treatment of hypercholesterolemia and ASCVD prevention.
|
28879791 |
2017 |
|
Hypercholesterolemia
|
0.700 |
Biomarker
|
disease |
BEFREE |
However, due to new lipid lowering drug developments like PCSK9-inhibitors (PCSK-9-I) a therapeutic algorithm for patients with severe hypercholesterolemia or isolated Lipoprotein(a)-hyperlipoproteinemia with progressive cardiovascular disease may be necessary to manage the use of PCSK9-I, lipoprotein apheresis (LA) or both.
|
29096860 |
2017 |
|
Hypercholesterolemia
|
0.700 |
GeneticVariation
|
disease |
BEFREE |
Polymorphisms in the proprotein convertase subtilisin/kexin type 9 (<i>PCSK9</i>) gene are associated with severe hypercholesterolemia and stroke.
|
28966647 |
2017 |
|
Hypercholesterolemia
|
0.700 |
Biomarker
|
disease |
BEFREE |
Interestingly, E2f1-/- mice fed a high-cholesterol diet (HCD) display a fatty liver phenotype and liver fibrosis, which is reversed by reexpression of PCSK9 in the liver.
|
28515357 |
2017 |
|
Hypercholesterolemia
|
0.700 |
Biomarker
|
disease |
BEFREE |
Inhibitory PCSK9 monoclonal antibodies are now prescribed to treat hypercholesterolemia.
|
27920219 |
2017 |
|
Hypercholesterolemia
|
0.700 |
Biomarker
|
disease |
BEFREE |
Population Pharmacokinetics (PK) and Pharmacodynamics (PD) Analysis of LY3015014, a Monoclonal Antibody to Protein Convertase Subtilisin/Kexin Type 9 (PCSK9) in Healthy Subjects and Hypercholesterolemia Patients.
|
27822850 |
2017 |
|
HYPERCHOLESTEROLEMIA, AUTOSOMAL DOMINANT, 3
|
0.700 |
CausalMutation
|
disease |
CLINVAR |
PCSK 9 gain-of-function mutations (R496W and D374Y) and clinical cardiovascular characteristics in a cohort of Turkish patients with familial hypercholesterolemia.
|
28777095 |
2017 |
|
HYPERCHOLESTEROLEMIA, AUTOSOMAL DOMINANT, 3
|
0.700 |
CausalMutation
|
disease |
CLINVAR |
Proprotein convertase subtilisin/kexin 9 V4I variant with LDLR mutations modifies the phenotype of familial hypercholesterolemia.
|
27206942 |
2017 |
|
Hypercholesterolemia
|
0.700 |
Biomarker
|
disease |
BEFREE |
Proprotein convertase subtilisin/kexin type 9 (PCSK9) decreases low-density lipoprotein (LDL) clearance, promotes hypercholesterolemia, and has recently emerged as a novel therapeutic target.
|
26824363 |
2016 |
|
Hypercholesterolemia
|
0.700 |
Biomarker
|
disease |
BEFREE |
Conversely, Pod-ATTAC mice and NTS-treated mice showed hypercholesterolemia and a 7- to 24-fold induction in plasma PCSK9.
|
27358438 |
2016 |
|
Hypercholesterolemia
|
0.700 |
Biomarker
|
disease |
BEFREE |
Significance of Monoclonal PCSK9-Antibodies - New Approaches to the Therapy of Hypercholesterolemia.
|
26789774 |
2016 |
|
Hypercholesterolemia
|
0.700 |
GeneticVariation
|
disease |
BEFREE |
We sequenced the LDLR 3' and 5' untranslated regions (UTR) and the PCSK9 5' UTR of 102 participants with moderate hypercholesterolemia in trial NCT01562080.
|
27015087 |
2016 |
|
Hypercholesterolemia
|
0.700 |
GeneticVariation
|
disease |
BEFREE |
Our objective was to determine the frequency of p.Leu167del mutation in APOE gene in subjects with autosomal dominant hypercholesterolemia (ADH) in whom LDLR, APOB, and PCSK9 mutations had been excluded and to identify the mechanisms by which this mutant apo E causes hypercholesterolemia.
|
27014949 |
2016 |
|
HYPERCHOLESTEROLEMIA, AUTOSOMAL DOMINANT, 3
|
0.700 |
GeneticVariation
|
disease |
CLINVAR |
Studies of the autoinhibitory segment comprising residues 31-60 of the prodomain of PCSK9: Possible implications for the mechanism underlying gain-of-function mutations.
|
27896130 |
2016 |
|
HYPERCHOLESTEROLEMIA, AUTOSOMAL DOMINANT, 3
|
0.700 |
GeneticVariation
|
disease |
CLINVAR |
Trafficking Dynamics of PCSK9-Induced LDLR Degradation: Focus on Human PCSK9 Mutations and C-Terminal Domain.
|
27280970 |
2016 |