Key result
Oxidative stress and lipid peroxidation products (E2-isoketal) potentiated inactivation of cardiac Na+ channels in cellular models, suggesting a mechanism for ischemia-related arrhythmias.
Population
Human embryonic kidney (HEK)-293 cells, cultured atrial (HL-1) myocytes, and a canine healing infarct model
Design
Preclinical
Authors
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May explain ischemia-related arrhythmias mechanistically; leaves open translation to human therapies.
Oxidative stress via lipid peroxidation reduces cardiac sodium channel availability, providing a potential molecular mechanism for ischemia-related conduction abnormalities and arrhythmias.
Fukuda et al. (2005) studied Myocardial ischemia and ventricular arrhythmias. Oxidative stress (tert-butyl-hydroperoxide and E2-isoketal) was evaluated on Cardiac Na+ channel availability and inactivation. Oxidative stress and lipid peroxidation products (E2-isoketal) potentiated inactivation of cardiac Na+ channels in cellular models, suggesting a mechanism for ischemia-related arrhythmias.
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