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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