title: TGF-beta in renal injury and disease.
abstract: Chronic progressive kidney diseases typically are characterized by loss of differentiated epithelial cells and activation of mesenchymal cell populations leading to renal fibrosis in response to a broad range of diverse renal injuries. Recent evidence has indicated that epithelial microinjury leads to unbalanced epithelial-mesenchymal communication to initiate the fibrotic response. Transforming growth factors beta constitute a large family of cytokines that control key cellular responses in development and tissue repair. Activation of autocrine and paracrine transforming growth factor-beta signaling cascades in the context of epithelial microinjuries initiate a variety of cell type-dependent signaling and activity profiles, including epithelial apoptosis and epithelial-to-mesenchymal transition, that trigger fibrogenic foci and initiate progressive fibrogenesis in chronic renal injury.
authors.affiliation: Department of Medicine, Mount Sinai School of Medicine, New York, NY 10029, USA. Erwin.Bottinger@mssm.edu
authors.forename: Erwin P
authors.initials: EP
authors.lastname: Böttinger
mesh_terms: D000818:Animals; D005355:Fibrosis / Q000473:pathology; D006801:Humans; D007674:Kidney Diseases / Q000378:metabolism* / Q000473:pathology* / Q000503:physiopathology; D008954:Models, Biological; D015398:Signal Transduction; D016212:Transforming Growth Factor beta / Q000037:antagonists & inhibitors / Q000378:metabolism* / Q000494:pharmacology / Q000502:physiology*
chemical_list: D016212:Transforming Growth Factor beta