Cardiovascular disease accounts for a large proportion of morbidity and mortality worldwide. We, and others, have shown that AP-1 transcription factors (TFs) play a role in remodeling the cardiomyocyte chromatin landscape in response to injury. Here, we aim to gain detailed insight into the molecular networks regulated by the AP-1 family of TFs during myocardial remodeling and regeneration, and determine whether we can rewire these networks to promote cardiomyocyte repair following injury and disease. Ultimately, our results will provide novel AP-1 targets that will serve as putative therapeutic targets to promote cardiac repair.
