Search results for "mitochondrial dysfunction"

showing 10 items of 14 documents

Aging-Related Disorders and Mitochondrial Dysfunction: A Critical Review for Prospect Mitoprotective Strategies Based on Mitochondrial Nutrient Mixtu…

2020

A number of aging-related disorders (ARD) have been related to oxidative stress (OS) and mitochondrial dysfunction (MDF) in a well-established body of literature. Most studies focused on cardiovascular disorders (CVD), type 2 diabetes (T2D), and neurodegenerative disorders. Counteracting OS and MDF has been envisaged to improve the clinical management of ARD, and major roles have been assigned to three mitochondrial cofactors, also termed mitochondrial nutrients (MNs), i.e., alpha-lipoic acid (ALA), Coenzyme Q10 (CoQ10), and carnitine (CARN). These cofactors exert essential-and distinct-roles in mitochondrial machineries, along with strong antioxidant properties. Clinical trials have mostly…

0301 basic medicineAgingAntioxidantUbiquinonemedicine.medical_treatmentmitochondrial nutrientsReviewoptic neuropathiesType 2 diabetesPharmacologyMitochondrionmedicine.disease_causeAntioxidantslcsh:Chemistrychemistry.chemical_compound0302 clinical medicineCardiovascular Diseaseoxidative stressaging-related disorderslcsh:QH301-705.5SpectroscopyThioctic AcidMitochondrial nutrientNeurodegenerative DiseasesGeneral MedicineComputer Science ApplicationsMitochondriaCardiovascular DiseasesAntioxidantmedicine.drugHumanCatalysisAging-related disorderCell LineInorganic Chemistry03 medical and health sciencesCarnitinemedicineAnimalsHumansMicrobiomeCarnitinePhysical and Theoretical ChemistryMolecular BiologyCoenzyme Q10business.industryAnimalOrganic ChemistryOxidative Stremedicine.diseaseClinical trial030104 developmental biologylcsh:Biology (General)lcsh:QD1-999chemistryDiabetes Mellitus Type 2MicrobiomeOptic neuropathiebusinessMitochondrial dysfunction030217 neurology & neurosurgeryOxidative stress
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Biological and biophysics aspects of metformin-induced effects: cortex mitochondrial dysfunction and promotion of toxic amyloid pre-fibrillar aggrega…

2016

The onset of Alzheimer disease (AD) is influenced by several risk factors comprising diabetes. Within this context, antidiabetic drugs, including metformin, are investigated for their effect on AD. We report that in the C57B6/J mice, metformin is delivered to the brain where activates AMP-activated kinase (AMPK), its molecular target. This drug affects the levels of β- secretase (BACE1) and β-amyloid precursor protein (APP), promoting processing and aggregation of β-amyloid (Aβ), mainly in the cortex region. Moreover, metformin induces mitochondrial dysfunction and cell death by affecting the level and conformation of Translocase of the Outer Membrane 40 (TOM40), voltage-dependent anion-sel…

0301 basic medicineAgingmedicine.medical_specialtyMitochondrial poreAmyloidTranslocase of the outer membraneContext (language use)AMP-Activated Protein KinasesBiologyAmyloid beta-Protein PrecursorMice03 medical and health sciences0302 clinical medicineβ-amyloid aggregationAlzheimer DiseaseHexokinaseInternal medicine?-amyloid aggregationmitochondrial dysfunctionmedicineAnimalsHypoglycemic Agentsmitochondrial poresMitochondrial transportAmyloid beta-PeptidesVoltage-Dependent Anion Channel 1BrainAMPKcell degenerationCell BiologyAlzheimer's diseasemedicine.diseaseMitochondriaMetformin030104 developmental biologyEndocrinologyAmyloid Precursor Protein SecretasesAlzheimer's diseasemetforminVDAC1030217 neurology & neurosurgeryResearch Papermedicine.drug
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Re-definition and supporting evidence toward Fanconi Anemia as a mitochondrial disease: Prospects for new design in clinical management

2021

Fanconi anemia (FA) has been investigated since early studies based on two definitions, namely defective DNA repair and proinflammatory condition. The former definition has built up the grounds for FA diagnosis as excess sensitivity of patients' cells to xenobiotics as diepoxybutane and mitomycin C, resulting in typical chromosomal abnormalities. Another line of studies has related FA phenotype to a prooxidant state, as detected by both in vitro and ex vivo studies. The discovery that the FA group G (FANCG) protein is found in mitochondria (Mukhopadhyay et al., 2006) has been followed by an extensive line of studies providing evidence for multiple links between other FA gene products and mi…

0301 basic medicineMitochondrial DNAMitochondrial DiseasesMitomycinMitochondrial diseaseClinical BiochemistryDiepoxybutaneReview ArticleMitochondrionBiologyBiochemistry03 medical and health scienceschemistry.chemical_compound0302 clinical medicineFanconi anemiaFANCGmedicineHumansClastogenCarnitinelcsh:QH301-705.5Coenzyme Q10lcsh:R5-920ProteinOrganic ChemistryMitochondrial nutrientProteinsmedicine.diseaseMitochondrial diseaseFanconi AnemiaPhenotypeClastogens030104 developmental biologylcsh:Biology (General)chemistryProoxidant stateCancer researchMitochondrial nutrientsMitochondrial dysfunctionlcsh:Medicine (General)030217 neurology & neurosurgeryHumanmedicine.drugRedox Biology
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Mitoprotective Clinical Strategies in Type 2 Diabetes and Fanconi Anemia Patients: Suggestions for Clinical Management of Mitochondrial Dysfunction

2020

Oxidative stress (OS) and mitochondrial dysfunction (MDF) occur in a number of disorders, and several clinical studies have attempted to counteract OS and MDF by providing adjuvant treatments against disease progression. The present review is aimed at focusing on two apparently distant diseases, namely type 2 diabetes (T2D) and a rare genetic disease, Fanconi anemia (FA). The pathogenetic links between T2D and FA include the high T2D prevalence among FA patients and the recognized evidence for OS and MDF in both disorders. This latter phenotypic/pathogenetic feature—namely MDF—may be regarded as a mechanistic ground both accounting for the clinical outcomes in both diseases, and…

0301 basic medicinePhysiologymedicine.medical_treatmentClinical Biochemistrymitochondrial nutrientsDiseaseType 2 diabetesReviewBioinformaticsmedicine.disease_causeBiochemistry03 medical and health scienceschemistry.chemical_compound0302 clinical medicineIn vivoFanconi anemiamitochondrial dysfunctionmedicineoxidative stressMolecular Biologyfanconi anemiaCoenzyme Q10business.industrylcsh:RM1-950Mitochondrial nutrientCell Biologymedicine.diseasePhenotype030104 developmental biologylcsh:Therapeutics. Pharmacologychemistry030220 oncology & carcinogenesisOxidative stretype 2 diabetesbusinessAdjuvantOxidative stressAntioxidants
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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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Antioxidant Alternatives in the Treatment of Amyotrophic Lateral Sclerosis: A Comprehensive Review

2020

Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease that produces a selective loss of the motor neurons of the spinal cord, brain stem and motor cortex. Oxidative stress (OS) associated with mitochondrial dysfunction and the deterioration of the electron transport chain has been shown to be a factor that contributes to neurodegeneration and plays a potential role in the pathogenesis of ALS. The regions of the central nervous system affected have high levels of reactive oxygen species (ROS) and reduced antioxidant defences. Scientific studies propose treatment with antioxidants to combat the characteristic OS and the regeneration of nicotinamide adenine dinucleotide (NAD+) lev…

0301 basic medicineamyotrophic lateral sclerosispterostilbenePterostilbenePhysiologyCentral nervous systemReviewPharmacologyNicotinamide adenine dinucleotidemedicine.disease_causelcsh:Physiology03 medical and health scienceschemistry.chemical_compound0302 clinical medicinePhysiology (medical)mitochondrial dysfunctionmedicineoxidative stressneurodegenerative diseasesAmyotrophic lateral sclerosisnicotinamide ribosidelcsh:QP1-981business.industryNeurodegenerationmedicine.disease030104 developmental biologymedicine.anatomical_structurechemistryNicotinamide ribosideNAD+ kinasebusiness030217 neurology & neurosurgeryOxidative stressFrontiers in Physiology
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Mitochondrial Dysfunction, Oxidative Stress and Neuroinflammation in Neurodegeneration with Brain Iron Accumulation (NBIA)

2020

The syndromes of neurodegeneration with brain iron accumulation (NBIA) encompass a group of invalidating and progressive rare diseases that share the abnormal accumulation of iron in the basal ganglia. The onset of NBIA disorders ranges from infancy to adulthood. Main clinical signs are related to extrapyramidal features (dystonia, parkinsonism and choreoathetosis), and neuropsychiatric abnormalities. Ten NBIA forms are widely accepted to be caused by mutations in the genes PANK2, PLA2G6, WDR45, C19ORF12, FA2H, ATP13A2, COASY, FTL1, CP, and DCAF17. Nonetheless, many patients remain without a conclusive genetic diagnosis, which shows that there must be additional as yet undiscovered NBIA gen…

0301 basic medicineautophagybrain iron accumulationPhysiologyNeurodegeneration with brain iron accumulationClinical BiochemistryChoreoathetosisrare diseaseReviewmedicine.disease_causeBiochemistryneuroinflammation03 medical and health sciences0302 clinical medicineWDR45lipid metabolismmitochondrial dysfunctionMedicineoxidative stressiron metabolismMolecular BiologyNeuroinflammationDystoniabusiness.industryParkinsonismlcsh:RM1-950Cell Biologymedicine.diseasePANK2030104 developmental biologylcsh:Therapeutics. Pharmacologymembrane remodellingmedicine.symptombusinessneurodegenerative disorderNeuroscience030217 neurology & neurosurgeryOxidative stressAntioxidants
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The Mitochondria-Targeted Antioxidant MitoQ Modulates Mitochondrial Function and Endoplasmic Reticulum Stress in Pancreatic β Cells Exposed to Hyperg…

2019

Background/aims Mitochondria-targeted antioxidants such as mitoquinone (MitoQ) have demonstrated protective effects against oxidative damage in several diseases. The increase in reactive oxygen species (ROS) production during glucose metabolism in β cells can be exacerbated under hyperglycaemic conditions such as type 2 diabetes (T2D), thus contributing to β cell function impairment. In the present work, we aimed to evaluate the effect of MitoQ on insulin secretion, oxidative stress, endoplasmic reticulum (ER) stress and nuclear factor kappa B (NFκB) signalling in a pancreatic β cell line under normoglycaemic (NG, 11.1 mM glucose), hyperglycaemic (HG, 25 mM glucose) and lipidic (palmitic ac…

0301 basic medicinemedicine.medical_specialtyPhysiologyUbiquinoneCarbohydrate metabolismmedicine.disease_causeMitoQlcsh:PhysiologyPancreatic β cellsAntioxidantsProinflammatory cytokinelcsh:Biochemistry03 medical and health scienceschemistry.chemical_compound0302 clinical medicineOrganophosphorus CompoundsInternal medicineCell Line TumorInsulin-Secreting CellsmedicineAnimalslcsh:QD415-436chemistry.chemical_classificationReactive oxygen speciesMitoQlcsh:QP1-981Endoplasmic reticulumGlutathioneEndoplasmic Reticulum StressType 2 DiabetesMitochondriaRatsOxidative Stress030104 developmental biologyEndocrinologyGlucosechemistry030220 oncology & carcinogenesisHyperglycemiaUnfolded protein responseER stressMitochondrial dysfunctionReactive Oxygen SpeciesOxidative stressSignal Transduction
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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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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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