Redox regulation of signal transduction in cardiac and smooth muscle.

In addition to the well-known property of reactive oxygen species (ROS) to cause non-specific cellular damage, the potential role of ROS in regulation of signal transduction has been recognized. Studies of vascular smooth muscle cells strongly suggest that ROS are required for cell growth signaling. The IP3-induced Ca2+ release from vascular smooth muscle can be selectively stimulated by ROS which may enhance signal transduction for muscle contraction and gene expression. The subunit-subunit contact within the ryanodine receptor complex, as well as intermolecular interactions between the ryanodine receptor and triadin, are redox sensitive, suggesting that ROS may regulate cardiac muscle Ca(2+)-signaling events. The biochemistry of ROS and thiol regulation may allow for specific interactions between ROS and target molecules during redox regulation.