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.
Current Projects
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
|
