Diabetic nephropathy (DN) is the leading cause of end-stage renal disease. The use of experimental models of DN has\r\nprovided valuable information regarding many aspects of DN, including pathophysiology, progression, implicated genes, and new\r\ntherapeutic strategies. A large number of mouse models of diabetes have been identified and their kidney disease was characterized\r\nto various degrees. Most experimental models of type 2 DN are helpful in studying early stages of DN, but these models have\r\nnot been able to reproduce the characteristic features of more advanced DN in humans such as nodules in the glomerular tuft or\r\nglomerulosclerosis. The generation of new experimental models of DN created by crossing, knockdown, or knockin of genes\r\ncontinues to provide improved tools for studying DN. These models provide an opportunity to search for new mechanisms\r\ninvolving the development of DN, but their shortcomings should be recognized as well. Moreover, it is important to recognize\r\nthat the genetic background has a substantial effect on the susceptibility to diabetes and kidney disease development in the various\r\nmodels of diabetes.
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