Our laboratory is interested in understanding how wound repair and scar formation are regulated at the cellular and molecular level. All organisms have a robust wound repair response involving the generation of new tissue and extracellular matrix (especially collagen) to replace what was damaged or lost. However, diseases such as atherosclerosis and fibrosis resemble wound repair gone wrong. We approach this question by studying platelet-derived growth factor (PDGF) signaling, which regulates the conversion of quiescent mural cells and fibroblasts into activated, matrix-producing cells called myofibroblasts. PDGF is important for normal wound repair and has been implicated in several chronic diseases involving scar tissue and fibrosis including atherosclerosis, scleroderma, and cancer. We are using a combination of tissue-specific mutation in mice, genetic background alteration, and lineage tracing to understand how scar formation occurs in disease and how it might be modulated to control disease. There is a tremendous need for new technology to solve the medical problems of fibrosis and atherosclerosis, and this can only come through a better understanding of the wound repair process.