title: Fibrogenesis of parenchymal organs.
abstract: Fibrosis of parenchymal organs is caused by prolonged injury, deregulation of the normal processes of wound healing, and extensive deposition of extracellular matrix (ECM) proteins. The current review will focus on common features of fibrogenesis in parenchymal organs, and will briefly discuss common features and differences in the pathophysiology of fibrosis. Comparison of hepatic, renal, and pulmonary fibrosis has identified several common mechanisms. Common themes include a critical role for the cytokine transforming growth factor beta and the generation of reactive oxygen species. Activated myofibroblasts are the common cell type that produce the excessive fibrous scar and may originate from endogenous cells such as hepatic stellate cells or fibroblasts, from the bone marrow such as fibrocytes, or from the transition of epithelial cells to mesenchymal cells. These concepts open new prospects for multidisciplinary research and the development of new therapies for fibrosis.
authors.affiliation: Department of Medicine, University of California, San Diego, La Jolla, California, USA.
authors.forename: Tatiana
authors.initials: T
authors.lastname: Kisseleva
authors.forename: David A
authors.initials: DA
authors.lastname: Brenner
mesh_terms: D003094:Collagen / Q000096:biosynthesis; D042783:Endothelial Cells / Q000378:metabolism / Q000502:physiology; D004847:Epithelial Cells / Q000378:metabolism / Q000502:physiology*; D005109:Extracellular Matrix / Q000378:metabolism; D005355:Fibrosis; D006801:Humans; D007249:Inflammation; D007668:Kidney / Q000473:pathology*; D008099:Liver / Q000473:pathology*; D008168:Lung / Q000473:pathology*; D053773:Transforming Growth Factor beta1 / Q000096:biosynthesis*; D014945:Wound Healing
chemical_list: D053773:Transforming Growth Factor beta1; D003094:Collagen