Each normal heart beat is triggered by an electrical impulse emitted from a group of specialized cardiomyocytes that together form the sinoatrial node (SAN). In this issue of the JCI, Swaminathan and colleagues demonstrate a new molecular mechanism that can disrupt the normal beating of the heart: angiotensin II - typically found in increased levels in heart failure and hypertension - oxidizes and activates Ca2+/calmodulin-dependent kinase II via NADPH oxidase activation, causing SAN cell death. The loss of SAN cells produces an electrical imbalance termed the "source-sink mismatch,"which may contribute to the SAN dysfunction that affects millions of people later in life and complicates a number of heart diseases.
CITATION STYLE
Huke, S., & Knollmann, B. C. (2011, August 1). Oxidized CaMKII: A “heart stopper” for the sinus node? Journal of Clinical Investigation. https://doi.org/10.1172/JCI58389
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