This review highlights that beyond their role in heart failure pathogenesis, endogenous reactive oxygen species are fundamental to the physiological regulation of acute cardiac contractility.
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Does not yet support altering ROS-targeted therapies clinically; extends understanding of endogenous ROS as physiological cardiac regulators.
Increased production of reactive oxygen species (ROS) has been linked to the pathogenesis of congestive heart failure. However, emerging evidence suggests the involvement of ROS in the regulation of various physiological cellular processes in the myocardium. In this review, we summarize the latest findings regarding the role of ROS in the acute regulation of cardiac contractility. We discuss ROS-dependent modulation of the inotropic responses to G protein-coupled receptor agonists (e.g. β-adrenergic receptor agonists and endothelin-1), the potential cellular sources of ROS (e.g. NAD(P)H oxidases and mitochondria) and the proposed end-targets and signalling pathways by which ROS affect contractility. Accumulating new data supports the fundamental role of endogenously generated ROS to regulate cardiac function under physiological conditions.
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Perjés et al. (2012) studied this question.
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