TGF-beta in renal injury and disease.
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.
Böttinger
Erwin P
EP
Department of Medicine, Mount Sinai School of Medicine, New York, NY 10029, USA. Erwin.Bottinger@mssm.edu
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*
D016212:Transforming Growth Factor beta