The Sucov lab uses advanced genetic and molecular strategies to identify pathways and processes that influence cardiomyocyte proliferation and heart regeneration, and the relation of these to heart physiology.
Common causes of adult heart injury are myocardial ischemia and infarction (heart attack), which result in cardiomyocyte cell death. In typical circumstances, this lost tissue is replaced by scar rather than by regenerated myocardium, which leads to compromised heart function and can progress to heart failure (the leading cause of death in the US and globally). In contrast, fetal and neonatal mammalian hearts can fully regenerate after injury, as can the adult heart in some nonmammalian species. We address fundamental questions about heart biology: what causes mammalian cardiomyocytes after birth to become postmitotic and nonregenerative, why does this occur, would there be detrimental consequences if adult hearts were more highly regenerative, can we use our insights to therapeutically improve regeneration after adult heart injury?
In a 2017 publication (Patterson et al., Nature Genetics 49:1346), we introduced a wholly new paradigm for adult heart regeneration to the field. Using a sophisticated genetic approach, we identified the cardiomyocyte subpopulation that is primarily responsible for regeneration, and identified genes that influence the tendency of these cardiomyocytes to divide or to become postmitotic. This work is the foundation for a large number of ongoing projects that seek to understand cardiomyocyte proliferation at multiple levels, including molecular signaling pathways, complex genetics (including human genetics), heart development, and adult heart physiology. Through our work, we discovered an unexpected link between heart regeneration and several adult heart diseases (arrhythmias and cardiomyopathies), and the nature of these relationships is an additional active area of investigation.