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pubmed:abstractText |
Most of the present knowledge on pathomechanism of renal fibrosis is based on experimental studies with laboratory animals. Today, a variety of genetic and inducible animal models that mimic primary causes of human disease such as diabetes mellitus, glomerulonephritis, or lupus erythematodes are available. However, only few of these models progress consistently to interstitial fibrosis in the kidney involving interestitial fibrosis, tubular atrophy, and glomerulosclerosis, which are common features of renal fibrogenesis. In this chapter, the mouse models of nephrotoxic serum nephritis, COL4A3-deficiency, and unilateral urethral obstruction, which all result reliably into renal fibrosis, are described.
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