BMP7 signaling in renal development and disease.
Fibrosis, and in particular tubulointerstitial fibrosis, is a common feature of almost all chronic renal diseases. Over the past several years, significant progress has been made in defining the underlying mechanisms of tubulointerstitial fibrosis. In a variety of mouse models, expression of transforming growth factor-beta is a primary causative factor which leads to increased numbers of myofibroblasts, collagen deposition and loss of tubular epithelia. More recently, another member of the transforming growth factor-beta superfamily, BMP7, was shown to counteract transforming growth factor-beta-mediated fibrosis. The activities of these secreted factors are regulated, in part, by extracellular ligand binding proteins which can enhance or suppress receptor ligand interactions.
Patel
Sanjeevkumar R
SR
Department of Internal Medicine, University of Michigan, Ann Arbor, MI 48109, USA.
Dressler
Gregory R
GR
D000818:Animals; D055419:Bone Morphogenetic Protein 7; D019485:Bone Morphogenetic Proteins / Q000378:metabolism*; D002352:Carrier Proteins / Q000378:metabolism; D004848:Epithelium / Q000378:metabolism; D005355:Fibrosis / Q000209:etiology / Q000378:metabolism; D006801:Humans; D007674:Kidney Diseases / Q000209:etiology / Q000378:metabolism*; D051379:Mice; D051381:Rats; D015398:Signal Transduction / Q000502:physiology*; D016212:Transforming Growth Factor beta / Q000378:metabolism*
C525819:BMP7 protein, human; C525821:Bmp7 protein, rat; D055419:Bone Morphogenetic Protein 7; D019485:Bone Morphogenetic Proteins; D002352:Carrier Proteins; D016212:Transforming Growth Factor beta; C501622:kielin-chordin-like protein, mouse