Although fibrosis can occur as part of normal wound healing, dysregulated fibrosis can affect almost any organ and results in severe dysfunction. Despite the variety of human disease of which this is a feature these diseases remain poorly understood due in part to the slow largely asymptomatic onset. Animal models are our only means to examine the early stages of these diseases. With them we can isolate perturbations in signaling pathways, chemokines and cytokines and study their effects. Here we summarize animal models that have been developed for the study of the most common human fibrotic conditions. We separate models of scleroderma and cirrhosis as the model development for each of these conditions face unique challenges. Although still imperfect, elegant solutions have been developed for modeling fibrosis in each. Indeed, progress in this area is currently rapid, and animal models will likely remain critical in moving forward our scientific understanding of these disease states.