Our research goals are broadly focused on understanding the mechanisms of cardiac and skeletal muscle adaptation to load under physiologic and pathologic conditions.

While the heart can grow in size to healthy levels, as seen in the athlete’s heart and during pregnancy, other pathologic etiologies such as hypertrophic cardiomyopathy (HCM), heart failure with reduced ejection fraction (HFrEF), long periods prolonged bed rest, and microgravity cause a detrimental mismatch between the mechanical capacity of the heart and the body’s hemodynamic demand. With heart failure, patients may receive left ventricular assist device (LVAD) to help sustain the weekend hearts. As such, the goal of the laboratory is to understand how muscle cells read and respond to internally and externally-driven changes in mechanical stimulation in the short and long term.

In particular, we are interested in answering the following questions:

1. What is the role of post-translational modification of structural proteins in cardiac muscle cells in response to mechanical unloading?
2. How does the activity of the ubiquitin-proteasome system change in response to mechanical unloading?
3. How does the balance between myofibrillogenesis and disassembly shape the muscle cell morphology and protein turnover?

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