Search results for "pcsk9"

showing 10 items of 74 documents

Insight into the Evolving Role of PCSK9

2022

Proprotein convertase subtilisin/kexin type 9 (PCSK9) is the last discovered member of the family of proprotein convertases (PCs), mainly synthetized in hepatic cells. This serine protease plays a pivotal role in the reduction of the number of low-density lipoprotein receptors (LDLRs) on the surface of hepatocytes, which leads to an increase in the level of cholesterol in the blood. This mechanism and the fact that gain of function (GOF) mutations in PCSK9 are responsible for causing familial hypercholesterolemia whereas loss-of-function (LOF) mutations are associated with hypocholesterolemia, prompted the invention of drugs that block PCSK9 action. The high efficiency of PCSK9 inhibitors (…

Endocrinology Diabetes and MetabolismPCSK9; cholesterol; anti-PCSK9; cardiovascular diseases; genetic; atherosclerosis; alirocumab; evolocumab; inclisiranMolecular BiologyBiochemistryMetabolites
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Identifying genetic risk variants for coronary heart disease in familial hypercholesterolemia: an extreme genetics approach

2015

Mutations in the low-density lipoprotein receptor (LDLR) gene cause familial hypercholesterolemia (FH), a disorder characterized by coronary heart disease (CHD) at young age. We aimed to apply an extreme sampling method to enhance the statistical power to identify novel genetic risk variants for CHD in individuals with FH. We selected cases and controls with an extreme contrast in CHD risk from 17 000 FH patients from the Netherlands, whose functional LDLR mutation was unequivocally established. The genome-wide association (GWA) study was performed on 249 very young FH cases with CHD and 217 old FH controls without CHD (above 65 years for males and 70 years of age for females) using the Ill…

AdultMaleRiskSettore MED/09 - Medicina InternaGenotypePopulationCoronary DiseaseSingle-nucleotide polymorphismGenome-wide association studyComorbidityFamilial hypercholesterolemiaQuantitative trait locusBiologymedicine.disease_causePolymorphism Single NucleotideArticleHyperlipoproteinemia Type IIYoung Adultsymbols.namesakeGene FrequencyRisk FactorsOdds RatioGeneticsmedicineHumansGenetic Predisposition to DiseaseeducationAllelesGenetics (clinical)AgedAged 80 and overGeneticsMutationeducation.field_of_studyfamilial hypercholesterolemiaPCSK9familial hypercholesterolemia; genetic risk factorgenetic risk factorGenetic VariationMiddle Agedmedicine.diseaseBonferroni correctionReceptors LDLCase-Control StudiesMutationsymbolsFemaleGenome-Wide Association StudyEuropean journal of human genetics
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Current insights into the German lipoprotein apheresis standard: PCSK9-inhibitors, lipoprotein apheresis or both?

2017

Abstract According to current European guidelines, lipid lowering therapy for progressive cardiovascular disease including cardiovascular events has to be focused on a target level for LDL-C. In contrast for Lp(a) a threshold has to be defined with respect to the method of measurement. 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. The therapeutic approach for patients with homozygous familial hypercholesterolemia i…

medicine.medical_specialtySerine Proteinase InhibitorsDiseaseFamilial hypercholesterolemia030204 cardiovascular system & hematologyRisk AssessmentHyperlipoproteinemia Type II03 medical and health sciencesTherapeutic approach0302 clinical medicineRisk FactorsInternal medicineGermanyInternal MedicinemedicineHumans030212 general & internal medicinePCSK9 Inhibitorsbiologybusiness.industryPCSK9Anticholesteremic AgentsPCSK9 InhibitorsGeneral MedicineLipoprotein(a)Cholesterol LDLmedicine.diseaseCombined Modality TherapyEndocrinologyTreatment OutcomeCardiovascular Diseasesbiology.proteinCardiologyBlood Component Removallipids (amino acids peptides and proteins)Proprotein Convertase 9Cardiology and Cardiovascular MedicinebusinessLipoprotein apheresisBiomarkersLipoproteinLipoprotein(a)Atherosclerosis. Supplements
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The Impact of the International Cooperation On Familial Hypercholesterolemia Screening and Treatment: Results from the ScreenPro FH Project

2019

Purpose of Review Familial hypercholesterolemia (FH) is often perceived and described as underdiagnosed and undertreated, though effective treatment of FH is available. Owing to the mentioned facts, it is ever more imperative to screen and treat FH patients. Subsequent to the identification of patients, the project focuses on the improvement of their prognoses. The ScreenPro FH project was established as a functional international network for the diagnosis, screening, and treatment of FH. Individual countries were assigned goals, e.g., to define the actual situation and available treatment. With “central support,” more centers and countries participated in the project. Subsequently, individ…

Pediatricsmedicine.medical_specialtyInternational CooperationFamilial hypercholesterolemiaFamilial hypercholesterolemia030204 cardiovascular system & hematologyTreatment resultsAntibodies Monoclonal HumanizedFHHyperlipoproteinemia Type II03 medical and health sciences0302 clinical medicineTotal cholesterolmedicineHumansMass ScreeningEffective treatment030212 general & internal medicineScreenPro FHLDL-CAlirocumabInternational networkEvidence-Based Medicine Clinical Trials and Their Interpretations (L. Roever Section Editor)business.industryAnticholesteremic AgentsIncidencePCSK9 InhibitorsScreen and treatmedicine.diseaseEvolocumab3. Good healthEuropeEvolocumabProprotein Convertase 9Cardiology and Cardiovascular MedicinebusinessDelivery of Health CareAlirocumabCurrent Atherosclerosis Reports
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P4573In patients with acute myocardial infarction, PCSK9 levels do not predict severity and recurrence of cardiovascular events

2019

Abstract Background In patients with coronary artery disease (CAD), it remains unclear whether serum PCSK9 levels can predict the severity of the disease and the risk of future cardiovascular events. Methods Among the patients admitted for an acute myocardial infarction (MI) from September 2015 to December 2016 in an intensive care unit from a university hospital, serum PCSK9 levels were measured on admission in patients not previously receiving statin therapy. We aimed to evaluate the association between PCSK9 levels, metabolic parameters, severity of CAD on coronary angiography, and the risk of in-hospital events and at one-year follow-up. Results In a total of 648 patients (mean age: 66 …

medicine.medical_specialtybusiness.industryPCSK9Internal medicineCardiologyMedicineMyocardial infarctionCardiology and Cardiovascular Medicinebusinessmedicine.diseaseEuropean Heart Journal
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The PCSK9 gene: a new gene controlling cholesterolemia

2007

The distribution of cholesterol plasma is regulated by complex interactions between genes and environmental factors. Mutations of PCSK9 gene seem to modulate the levels of LDLC. Mutations of PCSK9 gene with gain of function are associated to hypercholesterolemia and mutations with loss of function determine hypocholesterolemia.

PCSK9Settore MED/09 - Medicina Internahypercholesterolemiamutation
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Proprotein Convertase Subtilisin Kexin Type 9 Inhibition for Autosomal Recessive Hypercholesterolemia—Brief Report

2016

Objective— Proprotein convertase subtilisin kexin type 9 (PCSK9) inhibitors lower low-density lipoprotein (LDL) cholesterol in the vast majority of patients with autosomal dominant familial hypercholesterolemia. Will PCSK9 inhibition with monoclonal antibodies, in particular alirocumab, be of therapeutic value for patients with autosomal recessive hypercholesterolemia (ARH)? Approach and Results— Primary lymphocytes were obtained from 28 genetically characterized ARH patients and 11 controls. ARH lymphocytes treated with mevastatin were incubated with increasing doses of recombinant PCSK9 with or without saturating concentrations of alirocumab. Cell surface LDL receptor expression measured…

Male0301 basic medicineSettore MED/09 - Medicina Interna[SDV]Life Sciences [q-bio]receptorsalirocumabFamilial hypercholesterolemia030204 cardiovascular system & hematologyproprotein convertase subtilisin kexin type 90302 clinical medicinetherapeuticsLymphocytesCells CulturedhypercholesterolemiaAnticholesteremic AgentsPCSK9 InhibitorsAntibodies MonoclonalMiddle Aged3. Good healthPhenotypeAutosomal Recessive HypercholesterolemiaKexinDrug Therapy CombinationFemalelipids (amino acids peptides and proteins)LovastatinProprotein Convertase 9Cardiology and Cardiovascular Medicinemedicine.drugAdultmedicine.medical_specialtySerine Proteinase InhibitorsAdolescentBiologyAntibodies Monoclonal HumanizedLDLYoung Adult03 medical and health sciencesInternal medicinemedicineHumansGenetic Predisposition to DiseaseLovastatinAdaptor Proteins Signal TransducingAlirocumabPCSK9receptors LDLCholesterol LDLmedicine.diseaseProprotein convertasetherapeutic030104 developmental biologyEndocrinologyCase-Control Studiesalirocumab; hypercholesterolemia; proprotein convertase subtilisin kexin type 9; receptors LDL; therapeutics; Cardiology and Cardiovascular MedicineMutationLDL receptorHydroxymethylglutaryl-CoA Reductase InhibitorsArteriosclerosis, Thrombosis, and Vascular Biology
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Simultaneous Inhibition of Peripheral CB1R and iNOS Mitigates Obesity-Related Dyslipidemia Through Distinct Mechanisms.

2020

Diabetic dyslipidemia, characterized by increased plasma triglycerides and decreased HDL cholesterol levels, is a major factor contributing to nonalcoholic steatohepatitis and cardiovascular risk in type 2 diabetes. Activation of the cannabinoid-1 receptor (CB1R) and activation of inducible nitric oxide synthase (iNOS) are associated with nonalcoholic steatohepatitis progression. Here, we tested whether dual-targeting inhibition of hepatic CB1R and iNOS improves diabetic dyslipidemia in mice with diet-induced obesity (DIO mice). DIO mice were treated for 14 days with (S)-MRI-1867, a peripherally restricted hybrid inhibitor of CB1R and iNOS. (R)-MRI-1867, the CB1R-inactive stereoisomer that …

0301 basic medicineMaleVery low-density lipoproteinEndocrinology Diabetes and MetabolismNitric Oxide Synthase Type II[SDV.BC.IC] Life Sciences [q-bio]/Cellular Biology/Cell Behavior [q-bio.CB][SDV.BBM.BM] Life Sciences [q-bio]/Biochemistry Molecular Biology/Molecular biologyMice0302 clinical medicineReceptor Cannabinoid CB1[SDV.BC.IC]Life Sciences [q-bio]/Cellular Biology/Cell Behavior [q-bio.CB]Receptor[SDV.BBM.BC] Life Sciences [q-bio]/Biochemistry Molecular Biology/Biochemistry [q-bio.BM]Cells Cultured[SDV.MHEP.EM] Life Sciences [q-bio]/Human health and pathology/Endocrinology and metabolismbiology[SDV.MHEP.EM]Life Sciences [q-bio]/Human health and pathology/Endocrinology and metabolism[SDV.BBM.BC]Life Sciences [q-bio]/Biochemistry Molecular Biology/Biomolecules [q-bio.BM]Nitric oxide synthaseLiver[SDV.SP.PHARMA] Life Sciences [q-bio]/Pharmaceutical sciences/PharmacologyKexinlipids (amino acids peptides and proteins)medicine.medical_specialty[SDV.OT]Life Sciences [q-bio]/Other [q-bio.OT]LipoproteinsImmunoblotting030209 endocrinology & metabolismReal-Time Polymerase Chain Reaction03 medical and health sciencesInternal medicineCommentariesInternal MedicinemedicineAnimalsObesity[SDV.BBM.BC]Life Sciences [q-bio]/Biochemistry Molecular Biology/Biochemistry [q-bio.BM]Dyslipidemiasbusiness.industry[SDV.OT] Life Sciences [q-bio]/Other [q-bio.OT]PCSK9nutritional and metabolic diseases[SDV.MHEP.HEG]Life Sciences [q-bio]/Human health and pathology/Hépatology and Gastroenterology[SDV.BBM.BM]Life Sciences [q-bio]/Biochemistry Molecular Biology/Molecular biologymedicine.diseaseLipid Metabolism[SDV.MHEP.HEG] Life Sciences [q-bio]/Human health and pathology/Hépatology and GastroenterologyMice Inbred C57BL030104 developmental biologyEndocrinologyGlucoseLDL receptorbiology.proteinHepatocytes[SDV.SP.PHARMA]Life Sciences [q-bio]/Pharmaceutical sciences/PharmacologySteatosisbusinessDyslipidemia
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Efficacy and safety of adding alirocumab to rosuvastatin versus adding ezetimibe or doubling the rosuvastatin dose in high cardiovascular-risk patien…

2015

OBJECTIVE: To compare lipid-lowering efficacy of adding alirocumab to rosuvastatin versus other treatment strategies (NCT01730053).METHODS: Patients receiving baseline rosuvastatin regimens (10 or 20 mg) were randomized to: add-on alirocumab 75 mg every-2-weeks (Q2W) (1-mL subcutaneous injection via pre-filled pen); add-on ezetimibe 10 mg/day; or double-dose rosuvastatin. Patients had cardiovascular disease (CVD) and low-density lipoprotein cholesterol (LDL-C) ≥70 mg/dL (1.8 mmol/L) or CVD risk factors and LDL-C ≥100 mg/dL (2.6 mmol/L). In the alirocumab group, dose was blindly increased at Week 12 to 150 mg Q2W (also 1-mL volume) in patients not achieving their LDL-C target. Primary endpoi…

Monoclonal antibodymedicine.medical_specialtyTime FactorsSettore MED/09 - Medicina InternaInjections SubcutaneousHypercholesterolemiaUrology030204 cardiovascular system & hematologyPharmacologyAntibodies Monoclonal Humanizedlaw.inventionPCSK9Rosuvastatin03 medical and health sciences0302 clinical medicineDouble-Blind MethodEzetimibeRandomized controlled triallawmedicineClinical endpointHumansLow-density lipoprotein cholesterolRosuvastatinIn patient030212 general & internal medicineRosuvastatin CalciumAlirocumab; Ezetimibe; Low-density lipoprotein cholesterol; Monoclonal antibody; PCSK9; Rosuvastatin; Cardiology and Cardiovascular MedicineRetrospective StudiesAlirocumabDose-Response Relationship Drugbusiness.industryAnticholesteremic AgentsPCSK9Antibodies Monoclonalnutritional and metabolic diseasesCholesterol LDLEzetimibeRosuvastatin CalciumTreatment OutcomeCardiovascular DiseasesDrug Therapy CombinationHydroxymethylglutaryl-CoA Reductase InhibitorsbusinessCardiology and Cardiovascular MedicineFollow-Up StudiesAlirocumabmedicine.drugAtherosclerosis
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Reduced penetrance of autosomal dominant hypercholesterolemia in a high percentage of families: importance of genetic testing in the entire family.

2011

Abstract Background Autosomal dominant hypercholesterolemias (ADHs) are characterised by increased plasma levels of total and LDL cholesterol, predisposing to premature atherosclerosis. ADHs comprise several diseases with undistinguishable phenotype, caused by mutations in different genes: LDLR, APOB and PCSK9. Genetic studies are usually performed in patients with altered cholesterol levels. However, some persons carrying pathogenic mutations are normocholesterolemic and there are no further studies about this subject. We have studied the frequency of families and individuals carrying ADH mutations who do not present the disease in Spanish population. Methods We have analysed genes known t…

AdultMaleApolipoprotein BAdolescentFamilial hypercholesterolemiaBiologymedicine.disease_causeHyperlipoproteinemia Type IIChlorocebus aethiopsmedicineAnimalsHumansGenetic TestingChildGeneGenetic testingAgedApolipoproteins BGeneticsFamily HealthMutationmedicine.diagnostic_testurogenital systemPCSK9Serine EndopeptidasesCholesterol LDLSequence Analysis DNAMiddle Agedmedicine.diseasePenetrancePhenotypePedigreePhenotypeMutagenesisSpainApolipoprotein B-100COS CellsMutationbiology.proteinFemaleProprotein ConvertasesProprotein Convertase 9Cardiology and Cardiovascular Medicinehormones hormone substitutes and hormone antagonistsAtherosclerosis
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