Heart function and failure are controlled by
complex signaling and transcriptional networks that are just beginning
to be mapped out. My laboratory combines computational modeling and
live-cell microscopy to identify these molecular networks and understand
how they mediate cell decisions.
We are tackling a number of unexplained cellular decisions that are
fundamental to the development of heart failure. For example, after
myocardial infarction, what causes a given myocyte to choose enhanced
contractility, growth, or death? Why do certain stresses cause myocyte
lengthening, while other stresses increase myocyte thickness? Why are
certain forms of heart growth reversible while others are irreversible?
Answers to these basic science questions are being translated into novel
strategies to re-engineer the failing heart.
1) Compartmentation of cAMP/PKA signaling for cellular multitasking
2) High-throughput imaging and modeling of the cardiac hypertrophy signaling network
3) Crosstalk between beta-adrenergic signaling, Ca2+-dependent pathways, and cardiac arrhythmia