Exercise Training Prevents Oxidative Stress and Ubiquitin-Proteasome System Overactivity and Reverse Skeletal Muscle Atrophy in Heart Failure 英文参考文献.docVIP

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Exercise Training Prevents Oxidative Stress and Ubiquitin-Proteasome System Overactivity and Reverse Skeletal Muscle Atrophy in Heart Failure 英文参考文献.doc

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Exercise Training Prevents Oxidative Stress and Ubiquitin-Proteasome System Overactivity and Reverse Skeletal Muscle Atrophy in Heart Failure 英文参考文献

ExerciseTrainingPreventsOxidativeStressand Ubiquitin-ProteasomeSystemOveractivityandReverse SkeletalMuscleAtrophyinHeartFailure TelmaF.Cunha1,AlineV.N.Bacurau1,JoseB.N.Moreira1,NathalieA.Paixa?o1,JulianeC.Campos1, JulioC.B.Ferreira1,MarceloL.Leal2,CarlosE.Negra?o1,3,AnselmoS.Moriscot2,UlrikWisl?ff4, PatriciaC.Brum1* 1School ofPhysicalEducation andSport,UniversityofSa?o Paulo,Sa?o Paulo, Brazil, 2Biomedical SciencesInstitute,University ofSa?o Paulo,Sa?o Paulo,Brazil,3Heart Institute(InCor),UniversityofSa?o Paulo,Sa?o Paulo,Brazil,4K.G.JebsenCenterofExerciseinMedicine,NorwegianUniversityofScienceandTechnology,Trondheim, Norway Abstract Background: Heart failure (HF) is known to lead to skeletal muscle atrophy and dysfunction. However, intracellular mechanismsunderlyingHF-inducedmyopathyarenotfullyunderstood.WehypothesizedthatHFwouldincreaseoxidative stressandubiquitin-proteasomesystem(UPS)activationinskeletalmuscleofsympathetichyperactivitymousemodel.We alsotestedthehypothesisthataerobicexercisetraining(AET)wouldreestablishUPSactivationinmiceandhumanHF. Methods/Principal Findings: Time-course evaluation of plantaris muscle cross-sectional area, lipid hydroperoxidation, protein carbonylation and chymotrypsin-like proteasome activity was performed in a mouse model of sympathetic hyperactivity-inducedHF.Atthe7th monthofage,HFmicedisplayedskeletalmuscleatrophy,increasedoxidativestress andUPSoveractivation.Moderate-intensityAETrestoredlipidhydroperoxidesandcarbonylatedproteinlevelsparalleledby reducedE3ligasesmRNAlevels,andreestablishedchymotrypsin-likeproteasomeactivityandplantaristrophicity.Inhuman HF(patientsrandomizedtosedentaryormoderate-intensityAETprotocol),skeletalmusclechymotrypsin-likeproteasome activitywasalsoincreasedandAETrestoredittohealthycontrolsubjects’levels. Conclusions: Collectively, our data provide evidence that AET effectively counteracts redox imbalance and UPS overactivation,preventingskeletalmyopathyandexerciseintoleranceinsympathetichy