Fibrosis is a complex chronic disease characterized by a persistent repair response. Its pathogenesis is poorly understood but it is typically the result of chronic inflammation and maintained with the required activity of transforming growth factor-beta (TGF beta) and extracellular matrix (ECM) tension, both of which drive fibroblasts to transition into a myofibroblast phenotype. As the effector cells of repair, myofibroblasts migrate to the site of injury to deposit excessive amounts of matrix proteins and stimulate high levels of contraction. Myofibroblast activity is a decisive factor in whether a tissue is properly repaired by controlled wound healing or rendered fibrotic by deregulated repair. Extensive studies have documented the various contributing factors to an abrogated repair response. Though these fibrotic factors are known, very little is understood about the opposing antifibrotic molecules that assist in a successful repair, such as prostaglandin E2 (PGE(2)) and ECM retraction. The following review will discuss the general development of fibrosis through the transformation of myofibroblasts, focusing primarily on the prominent profibrotic pathways of TGF beta and ECM tension and antifibrotic pathways of PGE(2) and ECM retraction. The idea is to understand the ways in which the cell, after an injury and inflammatory response, normally controls its repair mechanisms through its homeostatic regulators so as to mimic them therapeutically to control abnormal pathways.