32 research outputs found
Ca2+ Sensitizing Troponin T Mutations Linked To Hypertrophic Cardiomyopathy Increase Apparent Cytosolic Ca2+ Binding
Genetically De-Sensitizing Myofilaments to Ca in a Mouse Model for Hypertrophic Cardiomyopathy Decreases Arrhythmia Incidence
Regional Connexin43 De-Phosphorylation and AMP-Kinase Activation after Rapid Pacing in Myofilament Ca Sensitized Hearts
Oxidized CaMKII: a “heart stopper” for the sinus node?
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