Please use this identifier to cite or link to this item: http://hdl.handle.net/10316/44868
Title: β-adrenergic over-stimulation and cardio-myocyte apoptosis: two receptors, one organelle, two fates?
Authors: Branco, Ana F 
Moreira, Ana C 
Cunha-Oliveira, Teresa 
Couto, Renata 
Sardao, Vilma A 
Rizvanov, Albert A 
Palotas, Andras 
Oliveira, Paulo J 
Keywords: Animals; Calcium; Catecholamines; Humans; Mitochondria; Myocytes, Cardiac; Reactive Oxygen Species; Receptors, Adrenergic, beta; Signal Transduction; Apoptosis
Issue Date: 2014
Project: info:eu-repo/grantAgreement/FCT/5876-PPCDTI/117912/PT 
PEst-C/SAU/LA0001/ 2013-2014 
CENTRO-07-ST24-FEDER-002008 
Serial title, monograph or event: Current drug targets
Volume: 15
Issue: 10
Abstract: 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 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.
URI: http://hdl.handle.net/10316/44868
Rights: openAccess
Appears in Collections:I&D CNC - Artigos em Revistas Internacionais

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