0000000000181895

AUTHOR

Emanuele Altomare

showing 3 related works from this author

Mitochondrial involvement in non-alcoholic steatohepatitis

2007

Non-alcoholic steatohepatitis (NASH) is an increasing recognized condition that may progress to end-stage liver disease. There are consistent evidences that mitochondrial dysfunction plays a central role in NASH whatever its origin. Mitochondria are the key controller of fatty acids removal and this is part of an intensive gene program that modifies hepatocytes to counteract the excessive fat storage. Mitochondrial dysfunction participates at different levels in NASH pathogenesis since it impairs fatty liver homeostasis and induces overproduction of ROS that in turn trigger lipid peroxidation, cytokines release and cell death. In this review we briefly recall the role of mitochondria in fat…

Mitochondrial DNAmedicine.medical_specialtyClinical BiochemistryBiologyMitochondrionModels BiologicalBiochemistryEnergy homeostasisAdenosine TriphosphateInternal medicinemedicineAnimalsHumansMolecular BiologyFatty liverGeneral MedicineTFAMLipid Metabolismmedicine.diseaseMitochondriaFatty LiverEndocrinologyMitochondrial respiratory chainMolecular MedicineSteatohepatitisSteatosisReactive Oxygen SpeciesMolecular Aspects of Medicine
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Uncoupling protein-2 (UCP2) induces mitochondrial proton leak and increases susceptibility of non-alcoholic steatohepatitis (NASH) liver to ischaemia…

2008

Background: The mechanisms of progression from fatty liver to steatohepatitis and cirrhosis are not well elucidated. Mitochondrial dysfunction represents a key factor in the progression of non-alcoholic steatohepatitis (NASH) as mitochondria are the main cellular site of fatty acid oxidation, ATP synthesis and reactive oxygen species (ROS) production. Aims: (1) To evaluate the role of the uncoupling protein 2 in controlling mitochondrial proton leak and ROS production in NASH rats and humans; and (2) to assess the acute liver damage induced by ischaemia–reperfusion in rats with NASH. Methods: Mitochondria were extracted from the livers of NASH humans and rats fed a methionine and choline de…

AdultMaleMitochondrial ROSmedicine.medical_specialtyMitochondria LiverMitochondrionBiologymedicine.disease_causeIon ChannelsMitochondrial ProteinsAdenosine TriphosphateInternal medicinemedicineAnimalsHumansUncoupling proteinUncoupling Protein 2Rats WistarBeta oxidationAdenosine TriphosphatasesMembrane Potential MitochondrialAldehydesFatty liverGastroenterologyMiddle Agedmedicine.diseaseRatsFatty LiverOxidative StressEndocrinologyMitochondrial respiratory chainLiverBiochemistryReperfusion InjuryAcute DiseaseDisease ProgressionFemaleSteatohepatitisReactive Oxygen SpeciesOxidative stressGut
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Targeting Mitochondria: A New Promising Approach for the Treatment of Liver Diseases

2010

Mitochondrial dysfunction acts as a common pathogenetic mechanism in several acute and chronic liver diseases, such as Alcoholic and Non-Alcoholic Fatty Liver Disease (NAFLD), drug-induced steatohepatitis, viral hepatitis, biliary cirrhosis, hepatocellular carcinoma, ischemia/reperfusion injury and transplant rejection. In particular mitochondrial uncoupling has been recently identified to play a determinant role in the pathogenesis of liver diseases by causing decrease of mitochondrial proton motive force and ATP depletion. Damaged mitochondria present defects in lipid homeostasis, bioenergetics impairment and overproduction of Reactive Oxygen Species (ROS), leading to lipid accumulation a…

Programmed cell deathMitochondrionBiologymedicine.disease_causeBiochemistryLiver diseaseDrug Delivery SystemsDrug DiscoverymedicineAnimalsHumansPharmacologychemistry.chemical_classificationReactive oxygen speciesCell DeathLiver DiseasesOrganic ChemistryFatty livermedicine.diseaseMitochondriaOxidative StressBiochemistrychemistryCancer researchMolecular MedicineSteatohepatitisReactive Oxygen SpeciesReperfusion injuryOxidative stressCurrent Medicinal Chemistry
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