Please use this identifier to cite or link to this item: http://hdl.handle.net/10316/44868
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dc.contributor.authorBranco, Ana F.-
dc.contributor.authorMoreira, Ana C.-
dc.contributor.authorCunha-Oliveira, Teresa-
dc.contributor.authorCouto, Renata-
dc.contributor.authorSardao, Vilma A.-
dc.contributor.authorRizvanov, Albert A.-
dc.contributor.authorPalotas, Andras-
dc.contributor.authorOliveira, Paulo J.-
dc.date.accessioned2017-12-10T15:36:21Z-
dc.date.available2017-12-10T15:36:21Z-
dc.date.issued2014-
dc.identifier.urihttp://hdl.handle.net/10316/44868-
dc.description.abstractNeuro-hormonal regulation of cardiac function via cathecol-amines results in increased heart rate and contractility. A persistent adrenergic tone, however, is an insult to the heart, affecting its regular homeostasis, altering morphology and gene expression patterns, as well as inducing apoptosis of cardio-myocytes. At the same time as being the main oxygen consumers, mitochondria are also key to the energy production required for the heart to maintain its vital functions and to integrate a series of signaling pathways that define the life and death of the cell. As α-adrenergic receptors (α-AR) orchestrate multiple biochemical events that can either trigger or inhibit cell death, mitochondria can act as a referee in the entire process. In fact, α-AR subtypes α1 and α2 activate various down-stream pathways which differently modulate intracellular calcium levels and production of mitochondrial reactive oxygen species (ROS). The delicate balance between an adaptive (cardio-protective) response resulting in increased contractility and activation of survival pathways, vs. cell death caused by calcium and ROS-induced mitochondrial disruption, along with evidence of their clinical and potential therapeutic translations, are reviewed in this communication.por
dc.description.sponsorshipFCTpor
dc.language.isoengpor
dc.relationinfo:eu-repo/grantAgreement/FCT/5876-PPCDTI/117912/PTpor
dc.relationPEst-C/SAU/LA0001/ 2013-2014por
dc.relationCENTRO-07-ST24-FEDER-002008por
dc.rightsopenAccesspor
dc.subjectAnimalspor
dc.subjectCalciumpor
dc.subjectCatecholaminespor
dc.subjectHumanspor
dc.subjectMitochondriapor
dc.subjectMyocytes, Cardiacpor
dc.subjectReactive Oxygen Speciespor
dc.subjectReceptors, Adrenergic, betapor
dc.subjectSignal Transductionpor
dc.subjectApoptosispor
dc.titleβ-adrenergic over-stimulation and cardio-myocyte apoptosis: two receptors, one organelle, two fates?por
dc.typearticle-
degois.publication.firstPage956por
degois.publication.lastPage964por
degois.publication.issue10por
degois.publication.titleCurrent drug targetspor
dc.relation.publisherversionhttp://www.eurekaselect.com/124321/articlepor
dc.peerreviewedyespor
degois.publication.volume15por
item.fulltextCom Texto completo-
item.languageiso639-1en-
item.grantfulltextopen-
crisitem.author.deptCNC - Center for Neuroscience and Cell Biology-
crisitem.author.deptInstitute of Interdisciplinary Research-
crisitem.author.researchunitCNC - Center for Neuroscience and Cell Biology-
crisitem.author.orcid0000-0002-7382-0339-
crisitem.author.orcid0000-0002-5201-9948-
Appears in Collections:I&D CNC - Artigos em Revistas Internacionais
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