Oxidized CaMKII: a "heart stopper" for the sinus node?

Huke S, Knollmann BC
J Clin Invest. 2011 121 (8): 2975-7

PMID: 21785211 · PMCID: PMC3148748 · DOI:10.1172/JCI58389

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.

MeSH Terms (15)

Angiotensin II Animals Apoptosis Calcium Calcium-Calmodulin-Dependent Protein Kinase Type 2 Cell Death Electrophysiology Heart Diseases Heart Failure Humans Mice Models, Biological NADPH Oxidases Oxygen Sinoatrial Node

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