Reactive oxygen species (ROS) induce cardiodepressant actions through ROS-dependent signaling events and post-translational modifications of myofilament proteins in the cardiac sarcomere.
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.
Sumandea et al. (Sat,) 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.