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lüll Oxidized CaMKII: a "heart stopper" for the sinus node?Huke S; Knollmann BCJ Clin Invest 2011[Aug]; 121 (8): 2975-7Each 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.|Angiotensin II/metabolism[MESH]|Animals[MESH]|Apoptosis[MESH]|Calcium-Calmodulin-Dependent Protein Kinase Type 2/*metabolism[MESH]|Calcium/metabolism[MESH]|Cell Death[MESH]|Electrophysiology/methods[MESH]|Heart Diseases/prevention & control/therapy[MESH]|Heart Failure[MESH]|Humans[MESH]|Mice[MESH]|Models, Biological[MESH]|NADPH Oxidases/metabolism[MESH]|Oxygen/*chemistry[MESH]|Sinoatrial Node/metabolism/*physiology[MESH] |