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EVIDENCE FOR THE REGULATION OF L‐TYPE Ca 2+ CHANNELS IN THE HEART BY REACTIVE OXYGEN SPECIES: MECHANISM FOR MEDIATING PATHOLOGY
Author(s) -
Hool Livia C
Publication year - 2008
Publication title -
clinical and experimental pharmacology and physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 103
eISSN - 1440-1681
pISSN - 0305-1870
DOI - 10.1111/j.1440-1681.2007.04727.x
Subject(s) - reactive oxygen species , oxidative stress , signal transduction , chemistry , microbiology and biotechnology , mitochondrion , oxidative phosphorylation , hydrogen peroxide , calcium channel , voltage dependent calcium channel , calcium , biochemistry , biology , organic chemistry
SUMMARY1 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 Ca 2+ 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.