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Tianjin Medical Journal ; (12): 1043-1047, 2014.
Article in Chinese | WPRIM | ID: wpr-458974

ABSTRACT

Cardiac contractile dysfunction and arrhythmic genesis are resulted from disturbed intracellular Na+and Ca2+ handling under condition of oxidation stress. Stress-induced intracellular signaling regulated mechanisms in which many activated stress kinases, such as cAMP-dependent protein kinase A, protein kinase C , Ca/calmodulin-dependent pro-tein kinaseⅡand classical pathways, are known to be involved. However, it is becoming increasingly evident that reactive oxygen species may directly oxidize these kinases, Na+and Ca2+channel protein and transporters, which lead to changing of intracellular Na+and Ca2+accumulation, and to trigger of arrhythmias.

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