Search results for "Lipids"

showing 10 items of 2228 documents

Docosahexaenoic Acid Attenuates Mitochondrial Alterations and Oxidative Stress Leading to Cell Death Induced by Very Long-Chain Fatty Acids in a Mous…

2020

In the case of neurodegenerative pathologies, the therapeutic arsenal available is often directed towards the consequences of the disease. The purpose of this study is, therefore, to evaluate the ability of docosahexaenoic acid (DHA), a molecule present in certain foods and considered to have health benefits, to inhibit the cytotoxic effects of very long-chain fatty acids (C24:0, C26:0), which can contribute to the development of some neurodegenerative diseases. The effect of DHA (50 &micro

0301 basic medicineProgrammed cell deathDocosahexaenoic AcidsCell SurvivalVery long chain fatty acidoligodendrocytesvery long-chain fatty acidmedicine.disease_causeCatalysisArticleCell Linelcsh:ChemistryInorganic Chemistry03 medical and health scienceschemistry.chemical_compoundMice0302 clinical medicinemedicineAnimalsViability assayPropidium iodidePhysical and Theoretical Chemistrylcsh:QH301-705.5Molecular BiologySpectroscopyMembrane Potential MitochondrialOrganic ChemistryAutophagyFatty Acidsfood and beveragesGeneral Medicinelipotoxicitydocosahexaenoic acidComputer Science ApplicationsCell biologyMitochondriaOligodendrogliaOxidative Stress030104 developmental biologylcsh:Biology (General)lcsh:QD1-999chemistryLipotoxicityDocosahexaenoic acidModels Animallipids (amino acids peptides and proteins)Reactive Oxygen Species030217 neurology & neurosurgeryOxidative stressInternational Journal of Molecular Sciences
researchProduct

BAG3 regulates total MAP1LC3B protein levels through a translational but not transcriptional mechanism

2015

Autophagy is mainly regulated by post-translational and lipid modifications of ATG proteins. In some scenarios, the induction of autophagy is accompanied by increased levels of certain ATG mRNAs such as MAP1LC3B/LC3B, ATG5 or ATG12. However, little is known about the regulation of ATG protein synthesis at the translational level. The cochaperone of the HSP70 system BAG3 (BCL2-associated athanogene 3) has been associated to LC3B lipidation through an unknown mechanism. In the present work, we studied how BAG3 controls autophagy in HeLa and HEK293 cells. Our results showed that BAG3 regulates the basal amount of total cellular LC3B protein by controlling its mRNA translation. This effect was …

0301 basic medicineProteasome Endopeptidase ComplexTranscription GeneticATG8ATG5BiologyBAG3ATG1203 medical and health sciences0302 clinical medicineProtein biosynthesisHumansRNA MessengerMolecular BiologyAdaptor Proteins Signal TransducingGeneticsGene knockdownAutophagyCell BiologyLipidsBasic Research PaperCell biologyHEK293 Cells030104 developmental biologyProtein BiosynthesisProteolysisApoptosis Regulatory ProteinsLysosomesMicrotubule-Associated ProteinsMAP1LC3B030217 neurology & neurosurgeryHeLa Cells
researchProduct

Border controls: Lipids control proteins and proteins control lipids.

2016

0301 basic medicineProtein FoldingChemistryCell MembraneBiophysicsMembrane ProteinsCell BiologyPlants010402 general chemistry01 natural sciencesBiochemistry0104 chemical sciences03 medical and health sciencesMembrane Lipids030104 developmental biologyEukaryotic CellsBiochemistryAnimalsHumansControl (linguistics)Biochimica et biophysica acta. Biomembranes
researchProduct

Lipid lowering nutraceuticals in clinical practice: position paper from an International Lipid Expert Panel.

2017

1.1. Cardiovascular disease and dyslipidemia: prevalence and global economic impact Cardiovascular diseases (CVDs) are the leading cause of mortality worldwide, reaching 31% of deaths in 2012 [1]. In particular, atherosclerosis and ischemic heart disease (IHD) are the main causes of premature death in Europe and are responsible for 42% of deaths in women and 38% in men under 75 years old [2]. The global economic impact of CVD is estimated to have been US $906 billion in 2015 and is expected to rise by 22% by 2030 [3]. Cardiovascular diseases also represent the major cause of disability in developed countries. It has been estimated that their growing burden could lead to a global increase in…

0301 basic medicineRED YEAST RICEDiseasePharmacologyPLACEBO-CONTROLLED TRIALchemistry.chemical_compound0302 clinical medicineCARDIOVASCULAR RISK-FACTORSFamily historyhealth care economics and organizationseducation.field_of_studyCONJUGATED LINOLEIC-ACIDOrvostudományokGeneral MedicinehumanitiesC-REACTIVE PROTEIN3. Good healthDENSITY-LIPOPROTEIN CHOLESTEROL030220 oncology & carcinogenesislipids (amino acids peptides and proteins)nutraceuticalLife Sciences & Biomedicineposition paperMODERATELY HYPERCHOLESTEROLEMIC SUBJECTSmedicine.medical_specialtyRANDOMIZED CONTROLLED-TRIALSeducationPopulationGuidelines/RecommendationsKlinikai orvostudományok03 medical and health sciencesMedicine General & InternallipidGeneral & Internal MedicineInternal medicineDiabetes mellitusmedicineCORONARY-HEART-DISEASERisk factoreducationFATTY LIVER-DISEASEScience & TechnologyCholesterolbusiness.industrydyslipidemia1103 Clinical Sciencesmedicine.disease030104 developmental biologychemistryrecommendationsEtiologybusinessDyslipidemiaArchives of medical science : AMS
researchProduct

Optimal use of lipid-lowering therapy after acute coronary syndromes: A Position Paper endorsed by the International Lipid Expert Panel (ILEP)

2021

Atherosclerotic cardiovascular disease (ASCVD) and consequent acute coronary syndromes (ACS) are substantial contributors to morbidity and mortality across Europe. Much of these diseases burden is modifiable, in particular by lipid-lowering therapy (LLT). Current guidelines are based on the sound premise that with respect to low density lipoprotein cholesterol (LDL-C), “lower is better for longer”, and the recent data have strongly emphasized the need of also “the earlier the better”. In addition to statins, which have been available for several decades, the availability of ezetimibe and inhibitors of proprotein convertase subtilisin/kexin type 9 (PCSK9) are additional very effective approa…

0301 basic medicineRMmedicine.medical_specialtyCombination therapyPCSK9 inhibitoreffectivenessTreatment goalsLipid-lowering therapy03 medical and health sciences0302 clinical medicineEzetimibemedicineHumansAcute Coronary SyndromeCombination therapyIntensive care medicinePharmacologyStatins.business.industryAtherosclerotic cardiovascular diseaseAnticholesteremic AgentsPCSK9StatinsEffectiveneDisease ManagementAtherosclerosisEzetimibeLipids030104 developmental biologyPCSK9 inhibitors030220 oncology & carcinogenesisPosition paperSafetybusinessVery high riskmedicine.drug
researchProduct

Invariant NKT Cells and Rheumatic Disease: Focus on Primary Sjogren Syndrome.

2019

Primary Sjogren syndrome (pSS) is a complex autoimmune disease mainly affecting salivary and lacrimal glands. Several factors contribute to pSS pathogenesis; in particular, innate immunity seems to play a key role in disease etiology. Invariant natural killer (NK) T cells (iNKT) are a T-cell subset able to recognize glycolipid antigens. Their function remains unclear, but studies have pointed out their ability to modulate the immune system through the promotion of specific cytokine milieu. In this review, we discussed the possible role of iNKT in pSS development, as well as their implications as future markers of disease activity.

0301 basic medicineReviewmedicine.disease_causeSalivary GlandsAutoimmunitylcsh:ChemistryPathogenesis0302 clinical medicinecytokineSjogren syndromelcsh:QH301-705.5innate immunitySpectroscopyautoimmunityLacrimal ApparatusGeneral MedicineNatural killer T cellComputer Science ApplicationsSjogren's SyndromeiNKTCatalysisInorganic Chemistry03 medical and health sciencesGlycolipidImmune systemAntigenstomatognathic systemRheumatic DiseasesmedicineAnimalsHumansPhysical and Theoretical ChemistryMolecular Biology030203 arthritis & rheumatologyAutoimmune diseaseInnate immune systembusiness.industryOrganic Chemistrymedicine.diseaseImmunity InnatecytokinesSettore MED/16 - Reumatologiastomatognathic diseases030104 developmental biologylcsh:Biology (General)lcsh:QD1-999ImmunologyNatural Killer T-CellsGlycolipidsbusinessInternational journal of molecular sciences
researchProduct

The Effect of Resveratrol on the Composition and State of Lipids and the Activity of Phospholipase A2 During the Excitation and Regeneration of Somat…

2019

It has been shown that in the somatic nerve's lipids, both during excitation and transection, changes occur with the composition of individual phospholipids and in phospholipids fatty acids, which changes the phase state of the myelin and nerve fiber axolemma lipid bilayer. A main contribution in the nerve degenerative processes is dependent on the composition phospholipid's fatty acid changes during the activation of both Ca2+-dependent and Ca2+-independent phospholipase A2 forms. At the same time, we studded changes in phosphoinisitol (PI) and diacylglycerol (DAG), which depend on the phosphoinositide cycle function during nerve excitation and degeneration processes. It was found that mye…

0301 basic medicineRhythmic excitationMyelinated nerve fiberPhysiologyPhospholipidNerve fiberresveratrollcsh:Physiology03 medical and health sciencesMyelinchemistry.chemical_compound0302 clinical medicinePhospholipase A2Physiology (medical)medicineskin and connective tissue diseasesphospholipidsDiacylglycerol kinasebiologylcsh:QP1-981Chemistrynerve intersectionmyelinated nerve fibersrhythmic excitation030104 developmental biologymedicine.anatomical_structurenervous system030220 oncology & carcinogenesisBiophysicsbiology.proteinlipids (amino acids peptides and proteins)Sciatic nervesense organsFrontiers in Physiology
researchProduct

The Absence of HIF-1α Increases Susceptibility to Leishmania donovani Infection via Activation of BNIP3/mTOR/SREBP-1c Axis

2020

Summary: Hypoxia-inducible factor-1 alpha (HIF-1α) is considered a global regulator of cellular metabolism and innate immune cell functions. Intracellular pathogens such as Leishmania have been reported to manipulate host cell metabolism. Herein, we demonstrate that myeloid cells from myeloid-restricted HIF-1α-deficient mice and individuals with loss-of-function HIF1A gene polymorphisms are more susceptible to L. donovani infection through increased lipogenesis. Absence of HIF-1α leads to a defect in BNIP3 expression, resulting in the activation of mTOR and nuclear translocation of SREBP-1c. We observed the induction of lipogenic gene transcripts, such as FASN, and lipid accumulation in inf…

0301 basic medicineSREBP-1cHIF1A Gene[SDV]Life Sciences [q-bio]Leishmania donovaniHIF-1αGeneral Biochemistry Genetics and Molecular BiologyMitochondrial Proteins03 medical and health sciences0302 clinical medicinevisceral leishmaniasisAnimalsHumansMyeloid Cellslcsh:QH301-705.5GenelipogenesisPI3K/AKT/mTOR pathwayDisease ResistanceMice Inbred BALB CInnate immune systembiologyIntracellular parasiteLipogenesisMacrophagesTOR Serine-Threonine KinasesGenetic VariationMembrane Proteinsbiology.organism_classificationLeishmaniaHypoxia-Inducible Factor 1 alpha SubunitFASNLipidsmacrophages3. Good healthCell biologyUp-RegulationMice Inbred C57BL030104 developmental biologylcsh:Biology (General)myeloid cellsLipogenesisLeishmaniasis VisceralDisease SusceptibilityacetateSterol Regulatory Element Binding Protein 1030217 neurology & neurosurgeryLeishmania donovaniSignal Transduction
researchProduct

Anti-PCSK9 treatment: is ultra-low low-density lipoprotein cholesterol always good?

2018

Anti-PCSK9 (proprotein convertase subtilisin kexin 9) monoclonal antibodies (Mab) are novel, potent lipid-lowering drugs. They demonstrated to improve the lipid profile in high cardiovascular risk patients. Anti-PCSK9 Mab inhibit the targeted low-density lipoprotein (LDL)-receptor degradation induced by PCSK9 protein and are able to reduce LDL cholesterol (LDL-C) levels on top of conventional lipid-lowering therapy. Though these drugs proved to be very safe in the short-term, little is known about the possible long-term effects, due to the short period of their marketing. The genetic low cholesterol syndromes (LCS) represent the natural models of the lipid-lowering anti-PCSK9 therapy, and a…

0301 basic medicineSerine Proteinase InhibitorsTime FactorsPhysiologymedicine.drug_class030204 cardiovascular system & hematologyPharmacologyMonoclonal antibodyRisk Assessment03 medical and health sciencesPCSK9 Genechemistry.chemical_compound0302 clinical medicineRisk FactorsPhysiology (medical)Diabetes mellitusmedicineAnimalsHumansDyslipidemiasmedicine.diagnostic_testbusiness.industryCholesterolPCSK9Anticholesteremic AgentsPCSK9 InhibitorsAntibodies MonoclonalCholesterol LDLmedicine.diseaseFatty LiverHypocholesterolemia030104 developmental biologyTreatment OutcomechemistryDiabetes Mellitus Type 2lipids (amino acids peptides and proteins)Proprotein Convertase 9Cardiology and Cardiovascular MedicineLipid profilebusinessCognition DisordersBiomarkersLipoproteinCardiovascular research
researchProduct

Characterization of a mutant form of human apolipoprotein B (Thr26_Tyr27del) associated with familial hypobetalipoproteinemia

2016

We have previously identified a deletion mutant of human apoB [apoB (Thr26_Tyr27del)] in a subject with primary hypobetalipoproteinemia. The present study determined the effect of Thr26_Tyr27del mutation on apoB secretion using transfected McA-RH7777 cells. Transient or stable transfection of apoB-48 containing the Thr26_Tyr27del mutation showed drastically reduced secretion of the mutant as compared to wild-type apoB-48. No lipoproteins containing the mutant apoB-48 were secreted into the medium. Incubation of transfected cells in a lipid-rich medium in the presence of cycloheximide showed rapid turnover of cell-associated mutant apoB-48 as compared to that of wild-type apoB-48. Immunofluo…

0301 basic medicineSettore MED/09 - Medicina InternaTime FactorsApolipoprotein B-48 secretionApolipoprotein BMutantDNA Mutational AnalysisApolipoprotein B mutation Apolipoprotein B-48 secretion Hypobetalipoproteinemia Proteasomal degradation030204 cardiovascular system & hematologymedicine.disease_causeEndoplasmic ReticulumHypobetalipoproteinemiaschemistry.chemical_compound0302 clinical medicineProteasomal degradationProteolysiSequence DeletionMutationbiologyMedicine (all)TransfectionProteasome InhibitorPhenotypeBiochemistryApolipoprotein B-100lipids (amino acids peptides and proteins)Proteasome InhibitorsHumanHeterozygoteProteasome Endopeptidase ComplexTime FactorCycloheximideTransfectiondigestive systemCell LineDNA Mutational Analysi03 medical and health sciencesmedicineHumansSecretionGenetic Predisposition to DiseaseMolecular BiologyEndoplasmic reticulumnutritional and metabolic diseasesCell Biologymedicine.diseaseMolecular biology030104 developmental biologychemistryProteolysisbiology.proteinHypobetalipoproteinemiaApolipoprotein B mutationApolipoprotein B-48Hypobetalipoproteinemia
researchProduct