title: Oxidized CaMKII: a "heart stopper" for the sinus node?
abstract: 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.
authors.forename: Sabine
authors.initials: S
authors.lastname: Huke
authors.forename: Björn C
authors.initials: BC
authors.lastname: Knollmann
mesh_terms: D000804:Angiotensin II / Q000378:metabolism; D000818:Animals; D017209:Apoptosis; D002118:Calcium / Q000378:metabolism; D054732:Calcium-Calmodulin-Dependent Protein Kinase Type 2 / Q000378:metabolism*; D016923:Cell Death; D004594:Electrophysiology / Q000379:methods; D006331:Heart Diseases / Q000517:prevention & control / Q000628:therapy; D006333:Heart Failure; D006801:Humans; D051379:Mice; D008954:Models, Biological; D019255:NADPH Oxidases / Q000378:metabolism; D010100:Oxygen / Q000737:chemistry*; D012849:Sinoatrial Node / Q000378:metabolism / Q000502:physiology*
chemical_list: D000804:Angiotensin II; D019255:NADPH Oxidases; D054732:Calcium-Calmodulin-Dependent Protein Kinase Type 2; D010100:Oxygen; D002118:Calcium