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dc.contributor.author | Branco A. | |
dc.contributor.author | Moreira A. | |
dc.contributor.author | Cunha-Oliveira T. | |
dc.contributor.author | Couto R. | |
dc.contributor.author | Sardão V. | |
dc.contributor.author | Rizvanov A. | |
dc.contributor.author | Palotás A. | |
dc.contributor.author | Oliveira P. | |
dc.date.accessioned | 2018-09-18T20:22:22Z | |
dc.date.available | 2018-09-18T20:22:22Z | |
dc.date.issued | 2014 | |
dc.identifier.issn | 1389-4501 | |
dc.identifier.uri | https://dspace.kpfu.ru/xmlui/handle/net/139195 | |
dc.description.abstract | © 2014 Bentham Science Publishers. Neuro-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 β-adrenergic receptors (β-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, β-AR subtypes β<inf>1</inf> and β<inf>2</inf> 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. | |
dc.relation.ispartofseries | Current Drug Targets | |
dc.subject | Apoptosis | |
dc.subject | Calcium | |
dc.subject | Cardio-myocyte | |
dc.subject | Mitochondria | |
dc.subject | Oxidative stress | |
dc.subject | β-adrenergic receptors | |
dc.title | β-adrenergic over-stimulation and cardio-myocyte apoptosis: Two receptors, one organelle, two fates? | |
dc.type | Article | |
dc.relation.ispartofseries-issue | 10 | |
dc.relation.ispartofseries-volume | 15 | |
dc.collection | Публикации сотрудников КФУ | |
dc.relation.startpage | 956 | |
dc.source.id | SCOPUS13894501-2014-15-10-SID84925936688 |