Key result
Reactive oxygen species (ROS) induce cardiodepressant actions through ROS-dependent signaling events and post-translational modifications of myofilament proteins in the cardiac sarcomere.
This review highlights the mechanistic role of reactive oxygen species in inducing post-translational modifications of sarcomeric proteins, which contributes to cardiac contractile dysfunction.
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ROS-mediated sarcomere modifications merit mechanistic research in HF; clinical translation remains untested.
Oxidative stress is common in many clinically important cardiac disorders, including ischemia/reperfusion, diabetes, and hypertensive heart disease. Oxidative stress leads to derangements in pump function due to changes in the expression or function of proteins that regulate intracellular Ca(2+) homeostasis. There is growing evidence that the cardiodepressant actions of reactive oxygen species (ROS) also are attributable to ROS-dependent signaling events in the sarcomere. This minireview focuses on myofilament protein post-translational modifications induced by ROS or ROS-activated signaling enzymes that regulate cardiac contractility.
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Sumandea et al. (2011) conducted a review in Cardiac disorders (ischemia/reperfusion, diabetes, hypertensive heart disease). Reactive oxygen species (ROS) induce cardiodepressant actions through ROS-dependent signaling events and post-translational modifications of myofilament proteins in the cardiac sarcomere.
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