Search results for "Mitochondrial Turnover"

showing 4 items of 4 documents

Mitochondrial oxidative injury: a key player in nonalcoholic fatty liver disease.

2020

Nonalcoholic fatty liver disease (NAFLD) has become the most prevalent liver disease worldwide. NAFLD is tightly linked to the metabolic syndrome, insulin resistance, and oxidative stress. Globally, its inflammatory form, nonalcoholic steatohepatitis (NASH), has become the main cause of liver-related morbidity and mortality, mainly due to liver cirrhosis and primary liver cancer. One hallmark of NASH is the presence of changes in mitochondrial morphology and function that are accompanied by a blocked flow of electrons in the respiratory chain, which increases formation of mitochondrial reactive oxygen species in a self-perpetuating vicious cycle. Consequences are oxidation of DNA bases and …

Liver Cirrhosismedicine.medical_specialtyMitochondrial DNAMitochondrial DiseasesPhysiologyMitochondrial TurnoverRespiratory chainBiologymedicine.disease_causedigestive system03 medical and health sciences0302 clinical medicineNon-alcoholic Fatty Liver DiseasePhysiology (medical)Internal medicineMitochondrial unfolded protein responseMitophagyNonalcoholic fatty liver diseasemedicineAnimalsHumans030304 developmental biology0303 health sciencesHepatologyGastroenterologynutritional and metabolic diseasesmedicine.diseasedigestive system diseases3. Good healthFatty LiverOxidative StressEndocrinologyMitochondrial biogenesis030211 gastroenterology & hepatologyOxidative stressAmerican journal of physiology. Gastrointestinal and liver physiology
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Compromising mitochondrial function with the antiretroviral drug efavirenz induces cell survival-promoting autophagy

2011

Hepatotoxicity is a very common side effect associated with the pharmacological treatment of human immunodeficiency virus (HIV) infection and its pathogenesis is poorly understood. Efavirenz (EFV) is the most widely used nonnucleoside reverse transcriptase inhibitor administered for the control of HIV and some of its toxic effects in hepatic cells have been recently shown to display features of mitochondrial dysfunction. Here we studied the activation of autophagy and, in particular, mitophagy, the main mitochondrial turnover mechanism, in human hepatic cells treated with clinically relevant concentrations of this drug. EFV-treated cells had altered mitochondria, characterized by a relative…

CyclopropanesEfavirenzHepatologyAnti-HIV AgentsCell SurvivalMitochondrial TurnoverAutophagyVacuoleMitochondrionBiologyBenzoxazinesMitochondriaCell biologychemistry.chemical_compoundchemistryApoptosisAlkynesMitophagyAutophagyCancer researchHepatic stellate cellHumansChemical and Drug Induced Liver InjuryHeLa CellsHepatology
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The role of mitochondrial oxidative stress in aging.

2003

Mitochondria are both a major source of oxidants and a target for their damaging effects, and, therefore, mitochondrial oxidative stress appears to be a cause, rather than a consequence, of cell aging. Oxidative damage in aging is particularly high in specific molecular targets, such as mitochondrial DNA and aconitase, and mitochondrial oxidative stress may drive tissue aging through intrinsic apoptosis. Mitochondrial function and morphology are impaired upon aging, as judged by a decline in membrane potential as well as by an increase in peroxide production and size of the organelles. In view of the age-related decreases in mitochondrial protein synthesis, mitochondrial transcripts, and ex…

SenescenceMitochondrial DNAAgingDNA RepairMitochondrial TurnoverMitochondrionBiologymedicine.disease_causeBiochemistryDNA MitochondrialGlutathioneMitochondriaOxygenOxidative StressBiochemistrymitochondrial fusionLiverPhysiology (medical)medicineDNAJA3AnimalsHumansReactive Oxygen SpeciesCell agingOxidative stressFree radical biologymedicine
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Mitochondrial biogenesis fails in secondary biliary cirrhosis in rats leading to mitochondrial DNA depletion and deletions

2011

Chronic cholestasis is characterizedby mitochondrial dysfunction, associated with loss of mitochondrialmembrane potential, decreased activities of respiratory chaincomplexes, and ATP production. Our aim was to determine themolecular mechanisms that link long-term cholestasis to mitochondrialdysfunction. We studied a model of chronic cholestasis inducedby bile duct ligation in rats. Key sensors and regulators of theenergetic state and mitochondrial biogenesis, mitochondrial DNA(mtDNA)-to-nuclear DNA (nDNA) ratio (mtDNA/nDNA) relativecopy number, mtDNA deletions, and indexes of apoptosis (BAX,BCL-2, and cleaved caspase 3) and cell proliferation (PCNA) wereevaluated. Our results show that long…

MaleMitochondrial DNAPhysiologyMitochondrial TurnoverMitochondrial HepatopathyNF-E2-Related Factor 1Respiratory chainMitochondria LiverProtein Serine-Threonine KinasesMitochondrionBiologyDNA MitochondrialSirtuin 1CholestasisProliferating Cell Nuclear AntigenPhysiology (medical)medicineAnimalsRats Wistarbcl-2-Associated X ProteinCholestasisHepatologyCaspase 3Liver Cirrhosis BiliaryGastroenterologyPyruvate Dehydrogenase Acetyl-Transferring KinaseRNA-Binding ProteinsTFAMmedicine.diseaseGA-Binding Protein Transcription FactorPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaMolecular biologyRatsGenes MitochondrialProto-Oncogene Proteins c-bcl-2Mitochondrial biogenesisChronic DiseaseBile DuctsGene DeletionTranscription FactorsAmerican Journal of Physiology-Gastrointestinal and Liver Physiology
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