Cardiac fibroblasts are the most prevalent cell type in the heart, but until recently have been disregarded in normal cardiac physiology. Now, evidence shows they actively regulates heart function even under normal conditions. The mechanisms of this regulation are poorly defined, and complicated by data being derived from multiple biological models. A systems biology approach is urgently required to understand cardiac fibroblast function. In this project, we explore the idea that cardiac fibroblasts regulate homeostasis in a two-stage process that includes senescence, and we propose new mathematical models to illuminate at the cellular level how and why the cardiac fibroblast is central to adult heart physiology under normal conditions.