Heart failure (HF) is a leading cause of mortality affecting over 6 million people in the United States. Cardiac fibrosis (CF) is a hallmark of HF causing decreased mechanical function of the heart, yet therapies attempting to directly target CF have not been clinically effective, demonstrating the need for greater understanding of fibrotic mechanisms during HF. Cardiac Fibroblasts (CFBs), the main drivers of CF are activated in HF by numerous stimuli and transform into myofibroblasts. These myofibroblasts then promote the development of CF through the production of excessive extracellular matrix (ECM) components. Cardiac inflammation co-exists with CF in HF, and T cell interactions with CFB result in a two-way crosstalk in which T cells induce CFB transformation, and CFB in turn function as non-professional antigen presenting cells that induce T cell activation. My work in the lab focuses on how the Aryl Hydrocarbon Receptor (AhR), a widely expressed transcription factor involved in responding to metabolic and environmental cues, functions in CFB transformation to myofibroblasts. Additionally, I am working on the newly appreciated role of CFBs as non-professional antigen presenting cells in the context of heart failure by studying both the induction of CFB MHC-II and its role in the activation of CFBs.
BS, Microbiology & Immunology; Biochemistry & Molecular Biology, University of Miami, Coral Gables, FL