Understanding the dual role of ROS in cardiac Ca2+ signaling could help harness their beneficial effects while preventing oxidative stress-induced arrhythmias and contractile dysfunction.
Dual ROS effects on Ca2+ signaling warrant caution with broad antioxidants; leaves open targeted modulation to preserve contractility and reduce arrhythmias.
Reactive oxygen species (ROS) are emerging as centre-stage players in cardiac functional regulation. ROS and Ca(2+) signals converge at dyads, the structural and functional units of cardiac excitation-contraction coupling. These two prominent signalling systems are intertwined with ROS modulation of the entire Ca(2+)-signalling network, and vice versa. While constitutively generated homoeostatic ROS are important in setting the redox potential of the intracellular milieu, dynamic signalling ROS shape microdomain and global Ca(2+) signals on both the beat-to-beat and greater time scales. However, ROS effects are complex and subtle, characterized by multiphasic and bidirectional Ca(2+) responses; and sustained oxidative stress may lead to compromised contractility and arrhythmogenicity. These new understandings should be leveraged to harness ROS for their beneficial roles while avoiding deleterious effects in the heart.
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Zhang et al. (2013) studied this question.
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