|
Diabetes Mellitus, Non-Insulin-Dependent
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Circulating PCSK9 levels are not associated with the conversion to type 2 diabetes.
|
31835041 |
2020 |
|
Prediabetes syndrome
|
0.030 |
Biomarker
|
disease |
BEFREE |
In ELSA-Brasil, a significant positive association between PCSK9 and worsening of glucose homeostasis, including the progression from normoglycemia to prediabetes, was found (OR (+1SD) 1.17 [1.04; 1.30], p = 0.0074).
|
31835041 |
2020 |
|
Hypercholesterolemia, Familial
|
0.500 |
Biomarker
|
disease |
BEFREE |
The efficacy of PCSK9 inhibitors in homozygous FH may be partly predicted by the LDLR variants.
|
31833051 |
2020 |
|
Cardiovascular Diseases
|
0.200 |
Biomarker
|
group |
BEFREE |
Cost-effectiveness analysis of PCSK9 inhibitors in cardiovascular diseases: a systematic review.
|
31832834 |
2019 |
|
Diabetes
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Interestingly, compared with ezetimibe, which was actively used as lipid-modifying therapy in the control group, PCSK9-mAbs seem to have a lower risk of incident diabetes (RR 0.60, 95% CI 0.37-0.99; p = 0.04).
|
31823301 |
2019 |
|
Diabetes Mellitus
|
0.100 |
GeneticVariation
|
group |
BEFREE |
Interestingly, compared with ezetimibe, which was actively used as lipid-modifying therapy in the control group, PCSK9-mAbs seem to have a lower risk of incident diabetes (RR 0.60, 95% CI 0.37-0.99; p = 0.04).
|
31823301 |
2019 |
|
Coronary Artery Disease
|
0.500 |
GeneticVariation
|
disease |
BEFREE |
Although lipid-lowering drugs, especially statins, and recently also PCSK9 inhibitors can reduce LDL cholesterol (LDL-C) and decrease the risk for cardiovascular disease (CVD) including coronary artery disease (CAD) events most efficiently, only 5-10% of high-risk cardiovascular patients reach the target values recommended by international guidelines.
|
31818446 |
2019 |
|
Cardiovascular Diseases
|
0.200 |
GeneticVariation
|
group |
BEFREE |
Although lipid-lowering drugs, especially statins, and recently also PCSK9 inhibitors can reduce LDL cholesterol (LDL-C) and decrease the risk for cardiovascular disease (CVD) including coronary artery disease (CAD) events most efficiently, only 5-10% of high-risk cardiovascular patients reach the target values recommended by international guidelines.
|
31818446 |
2019 |
|
Hypercholesterolemia
|
0.700 |
Biomarker
|
disease |
BEFREE |
L-IFPTA<sup>+</sup> vaccine could generate long-lasting, functional, and safe PCSK9-specific antibodies in C57BL/6 mice with severe atherosclerosis, which was accompanied by long-term therapeutic effect against hypercholesterolemia and atherosclerosis.
|
31818299 |
2019 |
|
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 |
|
Dyslipidemias
|
0.100 |
Biomarker
|
group |
BEFREE |
PCSK9 interferes with LDL metabolism and causes dyslipidemias in hematological malignancies particularly acute lymphoblastic leukemia.
|
31812013 |
2020 |
|
Liver carcinoma
|
0.050 |
Biomarker
|
disease |
BEFREE |
PCSK9 (Proprotein convertase Subtilisin/Kexin Type 9), an important regulator of lipid metabolism, has been shown to play a role in hepatocellular carcinoma by promoting metastasis.
|
31812013 |
2020 |
|
Neoplasm Metastasis
|
0.040 |
Biomarker
|
phenotype |
BEFREE |
PCSK9 (Proprotein convertase Subtilisin/Kexin Type 9), an important regulator of lipid metabolism, has been shown to play a role in hepatocellular carcinoma by promoting metastasis.
|
31812013 |
2020 |
|
Acute lymphocytic leukemia
|
0.010 |
AlteredExpression
|
disease |
BEFREE |
In the present study, PCSK9 expression was measured in acute lymphoblastic leukemia (ALL) patients and was found to be significantly induced.
|
31812013 |
2020 |
|
Childhood Acute Lymphoblastic Leukemia
|
0.010 |
AlteredExpression
|
disease |
BEFREE |
In the present study, PCSK9 expression was measured in acute lymphoblastic leukemia (ALL) patients and was found to be significantly induced.
|
31812013 |
2020 |
|
Hematologic Neoplasms
|
0.010 |
Biomarker
|
group |
BEFREE |
PCSK9 interferes with LDL metabolism and causes dyslipidemias in hematological malignancies particularly acute lymphoblastic leukemia.
|
31812013 |
2020 |
|
Adult Acute Lymphocytic Leukemia
|
0.010 |
AlteredExpression
|
disease |
BEFREE |
In the present study, PCSK9 expression was measured in acute lymphoblastic leukemia (ALL) patients and was found to be significantly induced.
|
31812013 |
2020 |
|
Precursor Cell Lymphoblastic Leukemia Lymphoma
|
0.010 |
Biomarker
|
disease |
BEFREE |
PCSK9 interferes with LDL metabolism and causes dyslipidemias in hematological malignancies particularly acute lymphoblastic leukemia.
|
31812013 |
2020 |
|
Hypercholesterolemia, Familial
|
0.500 |
GeneticVariation
|
disease |
BEFREE |
Autosomal dominant familial hypercholesterolemia (FH) is caused by mutations in LDLR,APOB and PCSK9.
|
31809983 |
2020 |
|
Hyperlipoproteinemia Type IIa
|
0.200 |
GeneticVariation
|
disease |
BEFREE |
Autosomal dominant familial hypercholesterolemia (FH) is caused by mutations in LDLR,APOB and PCSK9.
|
31809983 |
2020 |
|
Hypercholesterolemia, Familial
|
0.500 |
GeneticVariation
|
disease |
BEFREE |
Motivated by the FH mutation data on PCSK9, we found that modeling the PCSK9/LDLR interface revealed extensive electron delocalization between and within the protein partners.
|
31805108 |
2019 |
|
Hypocholesterolemia
|
0.200 |
GeneticVariation
|
disease |
BEFREE |
Mutations in PCSK9 that strengthen its interactions with LDLR result in familial hypercholesterolemia (FH) and early onset atherosclerosis, while nonsense mutations of PCSK9 result in cardio-protective hypocholesterolemia.
|
31805108 |
2019 |
|
Hyperlipoproteinemia Type IIa
|
0.200 |
GeneticVariation
|
disease |
BEFREE |
Motivated by the FH mutation data on PCSK9, we found that modeling the PCSK9/LDLR interface revealed extensive electron delocalization between and within the protein partners.
|
31805108 |
2019 |