TY - JOUR
T1 - Evidence For The Regulation Of L-Type Ca2+ Channels In The Heart by Reactive Oxygen Species: Mechanism For Mediating Pathology
AU - Hool, Livia
PY - 2008
Y1 - 2008
N2 - 1. It is well recognized that reactive oxygen species (ROS) can activate transduction pathways to mediate pathophysiology. An increase in ROS has been implicated in a number of cardiovascular disorders. Reactive oxygen species regulate cell function through redox modification of target proteins. One of these target proteins is the L-type Ca2+ channel.2. There is good evidence that thiol reducing and oxidizing compounds, including hydrogen peroxide, can influence calcium channel function. The evidence for regulation of the channel protein and regulatory proteins by thiol-specific modifying agents and relevance to hypoxia and oxidative stress is presented.3. Clinical studies suggest that calcium channel antagonists may be beneficial in reducing myocardial injury associated with oxidative stress. The identification of cysteines as possible targets for intervention during hypoxic trigger of arrhythmia or chronic pathological remodelling is discussed.
AB - 1. It is well recognized that reactive oxygen species (ROS) can activate transduction pathways to mediate pathophysiology. An increase in ROS has been implicated in a number of cardiovascular disorders. Reactive oxygen species regulate cell function through redox modification of target proteins. One of these target proteins is the L-type Ca2+ channel.2. There is good evidence that thiol reducing and oxidizing compounds, including hydrogen peroxide, can influence calcium channel function. The evidence for regulation of the channel protein and regulatory proteins by thiol-specific modifying agents and relevance to hypoxia and oxidative stress is presented.3. Clinical studies suggest that calcium channel antagonists may be beneficial in reducing myocardial injury associated with oxidative stress. The identification of cysteines as possible targets for intervention during hypoxic trigger of arrhythmia or chronic pathological remodelling is discussed.
U2 - 10.1111/j.1440-1681.2007.04727.x
DO - 10.1111/j.1440-1681.2007.04727.x
M3 - Article
C2 - 18197892
SN - 0305-1870
VL - 35
SP - 229
EP - 234
JO - Clinical and Experimental Pharmacology & Physiology
JF - Clinical and Experimental Pharmacology & Physiology
ER -