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Increased cardiac fibrosis is a characteristic remodeling response to stress-induced conditions in cardiovascular disease. Stress-induced transdifferentiation of fibroblasts is thought to be a critical step in the fibrotic pathway, but the understanding of the mechanism remains incomplete. Our lab has identified a role for the spectrin-based cytoskeleton in regulating this cardiac cell response to acute and chronic stress. In this study, tamoxifen-inducible fibroblast-specific βIV-spectrin knockout mice will be used to define the effects of BIV-spectrin deficiency in fibroblasts in regulating cardiac mechanical and electrical function. Cardiac function will be monitored using optical mapping, ex-vivo microscopy that maps electrical signals as they propagate across a heart. Additionally, immunoblots and quantitative PCR will be done to investigate protein expression and mRNA transcription regulation respectively. Results from this study will elucidate βIV–spectrin's role in fibrotic pathways leading to heart failure in fibroblasts.