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dc.contributor.authorRibeiro, Jr., R.F.
dc.contributor.authorDabkowski, E.R.
dc.contributor.authorShekar, K.C.
dc.date.accessioned2019-05-17T13:21:15Z
dc.date.available2019-05-17T13:21:15Z
dc.date.issued2018
dc.identifier.urihttps://www.scopus.com/inward/record.uri?eid=2-s2.0-85041399544&doi=10.1016%2fj.freeradbiomed.2018.01.012&partnerID=40&md5=82b45da745c1f26d2248e302e6e027ce
dc.identifier.urihttp://hdl.handle.net/10713/9169
dc.description.abstractHeart failure remains a major public-health problem with an increase in the number of patients worsening from this disease. Despite current medical therapy, the condition still has a poor prognosis. Heart failure is complex but mitochondrial dysfunction seems to be an important target to improve cardiac function directly. Our goal was to analyze the effects of MitoQ (100 µM in drinking water) on the development and progression of heart failure induced by pressure overload after 14 weeks. The main findings are that pressure overload-induced heart failure in rats decreased cardiac function in vivo that was not altered by MitoQ. However, we observed a reduction in right ventricular hypertrophy and lung congestion in heart failure animals treated with MitoQ. Heart failure also decreased total mitochondrial protein content, mitochondrial membrane potential in the intermyofibrillar mitochondria. MitoQ restored membrane potential in IFM but did not restore mitochondrial protein content. These alterations are associated with the impairment of basal and stimulated mitochondrial respiration in IFM and SSM induced by heart failure. Moreover, MitoQ restored mitochondrial respiration in heart failure induced by pressure overload. We also detected higher levels of hydrogen peroxide production in heart failure and MitoQ restored the increase in ROS production. MitoQ was also able to improve mitochondrial calcium retention capacity, mainly in the SSM whereas in the IFM we observed a small alteration. In summary, MitoQ improves mitochondrial dysfunction in heart failure induced by pressure overload, by decreasing hydrogen peroxide formation, improving mitochondrial respiration and improving mPTP opening. Copyright 2018en_US
dc.description.sponsorshipThis study was supported by grants from CNPq ( 455294/2014-3 ) and by the National Institutes of Health , Grant numbers HL074237 , HL101434 and HL072751 . Work in MPM's lab is supported by the Medical Research Council UK ( MC_U105663142 ) and by a Wellcome Trust Investigator award to MPM ( 110159/Z/15/Z )en_US
dc.description.urihttps://dx.doi.org/10.1016/j.freeradbiomed.2018.01.012en_US
dc.language.isoen_USen_US
dc.publisherElsevier Inc.en_US
dc.relation.ispartofFree Radical Biology and Medicine
dc.subjectHeart failureen_US
dc.subjectInterfibrillar mitochondriaen_US
dc.subjectMitochondrial dysfunctionen_US
dc.subjectMitoQen_US
dc.subjectReactive oxygen speciesen_US
dc.subjectSubsarcolemmal mitochondriaen_US
dc.titleMitoQ improves mitochondrial dysfunction in heart failure induced by pressure overloaden_US
dc.typeArticleen_US
dc.identifier.doi10.1016/j.freeradbiomed.2018.01.012
dc.identifier.pmid29421236


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