UCLA

There are tremendous health and financial burdens attributed to cardiovascular disease. The most common type, known as ischemic heart disease, is due to plaque buildup within the coronary arteries that supply the myocardium with oxygen and nutrients. Reduction or blockage of blood flow can lead to irreversible loss of cardiomyocytes, the main building blocks of the heart, with estimates placing that loss to upward of a billion cells. Despite medical therapy, the majority of patients eventually progress to heart failure, in which the main challenge for the development of therapeutic strategies is the limited regenerative ability of the adult mammalian heart. Our dissertation takes a multi-faceted approach in understanding cardiac regeneration and exploring whether neonatal systemic factors could be the gateway to a new therapy for ischemic heart disease. We report the development of a multi-colored mouse reporter system that enables deeper understanding of the cellular mechanisms driving early cardiac tissue formation. We apply a bioengineering approach to develop biodegradable and biocompatible nanoparticles as a new tool for clonal expansion analysis of cardiac cells. And lastly, we examined the proteomic profile of neonatal plasma in order to identify potential “pro-youthful” factors that may prevent irreversible myocardial damage. We hope that our body of work pushes forward the field of cardiac regeneration and sets the stage for the development of therapeutic interventions to prevent the progression to heart failure after an acute myocardial infarction.