Abstract

Fibrosis occurs as a part of normal wound healing. However, excessive or dysregulated fibrosis can lead to severe organ dysfunction and is a feature of a variety of diseases. Due to its insidious onset, fibrosis tends to go undetected in its early stages. This is in part why these diseases remain so poorly understood. Animal models have provided a means to examine these early stages and to isolate and understand the effect of perturbations in signaling pathways, chemokines, and cytokines. Here, we summarize recent progress in the understanding of the molecular pathogenesis of fibrosis, both its initiation and its maintenance phases, from animal models of fibrosis in the skin and liver. Due to these organs' properties, modeling fibrosis in them poses unique challenges. Elegant solutions have therefore been developed for modeling fibrosis in each, and now, great potential for animal models to contribute to our understanding appears scientifically imminent.

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