Search results for " mitochondrial dysfunction"

showing 4 items of 4 documents

Insulin resistance as common molecular denominator linking obesity to Alzheimer’s disease

2015

Alzheimer’s disease (AD) is an aging-related multi-factorial disorder to which metabolic factors contribute at what has canonically been considered a centrally mediated process. Although the exact underlying mechanisms are still unknown, obesity is recognized as a risk factor for AD and the condition of insulin resistance seems to be the link between the two pathologies. Using mice with high fat diet (HFD) obesity we dissected the molecular mechanisms shared by the two disorders. Brains of HFD fed mice showed elevated levels of APP and Aβ 40 /Aβ 42 together with BACE, GSK3β and Tau proteins involved in APP processing and Aβ accumulation. Immunofluorescence, Thioflavin T staining experiments…

Malemedicine.medical_specialtyTime FactorsAdipokineAmyloidogenic ProteinsInflammationBiologyDiet High-Fatmedicine.disease_causeAdipokines Alzheimer’s disease gene expression inflammation insulin resistance mitochondrial dysfunction obesity.Settore BIO/09 - FisiologiaGlycogen Synthase Kinase 3MiceInsulin resistanceAlzheimer DiseaseInternal medicinemedicineAnimalsInsulinObesityReceptorGSK3BGlycogen Synthase Kinase 3 betaSettore BIO/16 - Anatomia UmanaNeurodegenerationBrainmedicine.diseaseReceptor InsulinMice Inbred C57BLDisease Models AnimalOxidative StressInsulin receptorEndocrinologyGene Expression RegulationNeurologyCase-Control Studiesbiology.proteinCytokinesNeurology (clinical)Amyloid Precursor Protein SecretasesInsulin Resistancemedicine.symptomOxidative stressSignal Transduction
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Vascular ageing and endothelial cell senescence: Molecular mechanisms of physiology and diseases

2016

Ageing leads to a progressive deterioration of structure and function of all organs over the time. During this process endothelial cells undergo senescence and manifest significant changes in their properties, resulting in impairment of the vascular functionality and neo-angiogenic capability. This ageing-dependent impairment of endothelial functions is considered a key factor contributing to vascular dysfunctions, which is responsible of several age-related diseases of the vascular system and other organs. Several mechanisms have been described to control ageing-related endothelial cell senescence including microRNAs, mitochondrial dysfunction and micro environmental stressors, such as hyp…

0301 basic medicineSenescenceAgingEndotheliump73Biologymedicine.disease_cause03 medical and health sciencesEndotheliocyte; Endothelium; Hypoxia; MicroRNAs; Mitochondrial dysfunction; Oxidative stress; P53 family; P73; Transglutaminase 2; VEGF; Aging; Developmental BiologymicroRNAmedicineAnimalsHumansSettore MED/05 - Patologia ClinicaEndotheliocyte; Endothelium; Hypoxia; Mitochondrial dysfunction; Oxidative stress; Transglutaminase 2; VEGF; microRNAs; p53 family; p73Vascular DiseasesEndotheliumHypoxiaCellular SenescenceEndothelial CellsMicroRNASettore MED/23 - Chirurgia CardiacaBECN1Hypoxia (medical)VEGFMitochondriamicroRNAsEndothelial stem cellTransglutaminase 2030104 developmental biologymedicine.anatomical_structureOxidative stressAgeingImmunologyOxidative stremedicine.symptomMitochondrial dysfunctionp53 familyEndotheliocyteNeuroscienceOxidative stressDevelopmental BiologyMechanisms of Ageing and Development
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Fructose-1,6-Bisphosphate Protects Hippocampal Rat Slices from NMDA Excitotoxicity

2019

Effects of fructose 1,6-bisphosphate (F-1,6-P2) towards N-methyl-d-aspartate NMDA excitotoxicity were evaluated in rat organotypic hippocampal brain slice cultures (OHSC) challenged for 3 h with 30 &mu

Fructose 16-bisphosphateExcitotoxicityFructose-bisphosphate aldolaseorganotypic hippocampal brainslice culturesmedicine.disease_causeHippocampuslcsh:Chemistrychemistry.chemical_compoundenergymetabolismFructose-Bisphosphate Aldolaseenergy metabolismfructose-16-bisphosphatelcsh:QH301-705.5Spectroscopy<i>N</i>-methyl-<span style="font-variant: small-caps">d</span>-aspartatebiologyChemistryorganotypic hippocampal brain slice culturesGlyceraldehyde-3-Phosphate DehydrogenasesGeneral MedicineComputer Science ApplicationsFructose-BisphosphataseNeuroprotective AgentsNMDA receptorexcitotoxicityPhosphofructokinaseN-methyl-d-aspartatemedicine.medical_specialtyN-MethylaspartateFructose 16-bisphosphataseCatalysisArticleInorganic ChemistryNecrosisInternal medicinemitochondrial dysfunctionmedicineAnimalsPhysical and Theoretical ChemistryRats WistarMolecular BiologySettore BIO/10 - BIOCHIMICAOrganic ChemistryAldolase AMetabolismPurine NucleosidesRatsEndocrinologylcsh:Biology (General)lcsh:QD1-999Phosphofructokinases6-bisphosphatebiology.proteinfructose-1; 6-bisphosphate; N-methyl-d-aspartate; excitotoxicity; energymetabolism; mitochondrial dysfunction; organotypic hippocampal brainslice culturesfructose-1
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From clinical description, to in vitro and animal studies, and backward to patients: Oxidative stress and mitochondrial dysfunction in Fanconi anemia

2013

Fanconi anemia (FA) is a rare genetic disease associated with deficiencies in DNA repair pathways. A body of literature points to a pro-oxidant state in FA patients, along with evidence for oxidative stress (OS) in the FA phenotype reported by in vitro, molecular, and animal studies. A highlight arises from the detection of mitochondrial dysfunction (MDF) in FA cell lines of complementation groups A, C, D2, and G. As yet lacking, in vivo studies should focus on FA-associated MDF, which may help in the understanding of the mitochondrial basis of OS detected in cells and body fluids from FA patients. Beyond the in vitro and animal databases, the available analytical devices may prompt the dir…

Pathologymedicine.medical_specialtyDNA RepairFree RadicalsDNA repairmitochondrial nutrientsCell Cycle ProteinsFree radicalsDiseaseBiologymedicine.disease_causeBioinformaticsBiochemistryChemopreventionPathogenesis03 medical and health sciencesMice0302 clinical medicineIn vivoFanconi anemiaPhysiology (medical)medicineAnimalsHumans030304 developmental biology0303 health sciencesMitochondrial nutrientNuclear ProteinsFanconi anemia Mitochondrial dysfunction Mitochondrial nutrients Chemoprevention Free radicalsmedicine.diseasePhenotype3. Good healthMitochondriaOxidative StressFanconi Anemia030220 oncology & carcinogenesisFanconi anemiaAnimal studiesReactive Oxygen SpeciesMitochondrial dysfunctionOxidative stress
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