β-Adrenergic Over-Stimulation and Cardio-Myocyte Apoptosis: Two Receptors, One Organelle, Two Fates?

Author(s): Ana F. Branco, Ana C. Moreira, Teresa Cunha-Oliveira, Renata Couto, Vilma A. Sardao, Albert A. Rizvanov, Andras Palotas, Paulo J. Oliveira

Journal Name: Current Drug Targets

Volume 15 , Issue 10 , 2014

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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.

Keywords: Apoptosis, α-adrenergic receptors, calcium, cardio-myocyte, mitochondria, oxidative stress.

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Article Details

VOLUME: 15
ISSUE: 10
Year: 2014
Page: [956 - 964]
Pages: 9
DOI: 10.2174/1389450115666140902124230
Price: $65

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