Our Research
Turning "on and off" cardiomyocyte contraction
Neuroregulation of cardiac development
The role of cardiac innervation during heart development remains unclear. Our research aims to determine the effect of sympathetic innervation on postnatal cardiac maturation with a focus on heart regeneration and disease development. To this end, we recently demonstrated that sympathetic neurons regulate clock genes to limit mitosis entry in postnatal cardiomyocytes.
Transcriptional enhancers as key disease modifiers in heart failure
Heart failure is the leading cause of death worldwide. Genome-wide association studies have linked cardiac phenotypes with distant-acting transcriptional enhancers. However, despite the abundance of cardiac enhancers and their significance for disease, their role and mechanistic contribution to cardiac disease remain unknown. We sought to investigate the role of cardiac enhancers in the development of heart failure using stem cell-derived cardiomyocytes and animal models.
Generating a “power switch” to examine the mechanism of heart regenerative therapies
Ischemic heart disease resulting in heart failure is the number one cause of death worldwide. A major new treatment is the use of stem cells to regenerate damaged muscle. A core question regarding regenerative treatment strategies is whether any new cardiomyocytes can integrate with the myocardium and mature sufficiently to provide physiologically relevant contraction. To answer this question, we have generated a novel system wherein contraction is genetically regulated in stem cell-derived cardiomyocytes.
Funding Sources
