TGF-β and fibrosis |
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Authors: | Mary H Branton Jeffrey B Kopp |
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Institution: | Kidney Disease Section, Metabolic Diseases Branch, NIDDK, National Institutes of Health, Bethesda, MD 20892–1268, USA |
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Abstract: | Transforming growth factor-beta (TGF-β) isoforms are multifunctional cytokines that play a central role in wound healing and in tissue repair. TGF-β is found in all tissues, but is particularly abundant in bone, lung, kidney and placental tissue. TGF-β is produced by many but not all parenchymal cell types, and is also produced or released by infiltrating cells such as lymphocytes, monocytes/macrophages, and platelets. Following wounding or inflammation, all these cells are potential sources of TGF-β. In general, the release and activation of TGF-β stimulates the production of various extracellular matrix proteins and inhibits the degradation of these matrix proteins, although exceptions to these principles abound. These actions of TGF-β contribute to tissue repair, which under ideal circumstances leads to the restoration of normal tissue architecture and may involve a component of tissue fibrosis. In many diseases, excessive TGF-β contributes to a pathologic excess of tissue fibrosis that compromises normal organ function, a topic that has been the subject of numerous reviews 1, 2 and 3]. In the following chapter, we will discuss the role of TGF-β in tissue fibrosis, with particular emphasis on renal fibrosis. |
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Keywords: | TGF-β glomerulosclerosis diabetic nephropathy renal interstitial fibrosis extracellular matrix matrix metalloproteinase angiotensin |
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