CaMKII-Dependent Regulation of Atrial Late Sodium Current and Excitability
Oct 4th, 2017 by ajphearteditor
What is the interplay between late sodium current and Ca2+/calmodulin-dependent protein kinase II (CaMKII) in the early stages of atrial fibrillation induced by abnormal focal activity? Listen as Consulting Editor Igor Efimov (George Washington University) interviews lead author Thomas Hund (The Ohio State University) and content expert Patrick Boyle (Johns Hopkins University) about the unique modeling study by Onal et al. Hund and co-authors created a model focused on the CaMKII signaling pathway, itself dramatically altered in patients with atrial fibrillation, to piece together the sequence of events and mechanisms which trigger atrial arrhythmias. Hund and collaborators became interested in how CaM kinase II regulates the voltage-gated sodium channel, and their model allows for the cell to respond to various stimuli. Listen as our experts discuss how cell models portend the future of tissue-scale modeling (including a reference to the movie Jaws) and the necessity of balancing layers of complexity with the need for simplicity to maintain the integrity of the model.
Birce Onal, Daniel Gratz, Thomas J Hund Ca2+/calmodulin kinase II-dependent regulation of atrial myocyte late Na+ current, Ca2+ cycling and excitability: a mathematical modeling study Am J Physiol Heart Circ Physiol, published August 25, 2017. DOI: 10.1152/ajpheart.00185.2017