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10.1152/ajprenal.90421.2008 http://scihub22266oqcxt.onion/10.1152/ajprenal.90421.2008 18784259!ä!18784259 Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=18784259&cmd=llinks): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 215 Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\18784259.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Am+J+Physiol+Renal+Physiol 2009 ; 296 (2): F213-29 Nephropedia Template TP {{tp|p=18784259|t=2009. Inducible rodent models of acquired podocyte diseases |pdf=|usr=}}{{18784259}} gab.com Text Inducible rodent models of acquired podocyte diseases JO: Am J Physiol Renal Physiol http://www.kidney.de/pget.php?&tw=1&pmid=18784259 #FOAvip Glomerular diseases remain the leading cause of chronic and end-stage kidney disease. Significant advances in our understanding of human glomerular diseases have been enabled by the development and better characterization of animal models. Diseases of the glomerular epithelial cells (podocytes) account for the majority of proteinuric diseases. Rodents have been extensively used experimentally to better define mechanisms of disease induction and progression, as well as to identify potential targets and therapies. The development of podocyte-specific genetically modified mice has energized the research field to better understand which animal models are appropriate to study acquired podocyte diseases. In this review we discuss inducible experimental models of acquired nondiabetic podocyte diseases in rodents, namely, passive Heymann nephritis, puromycin aminonucleoside nephrosis, adriamycin nephrosis, liopolysaccharide, crescentic glomerulonephritis, and protein overload nephropathy models. Details are given on the model backgrounds, how to induce each model, the interpretations of the data, and the benefits and shortcomings of each. Genetic rodent models of podocyte injury are excluded. Twit Text FOAVip Inducible rodent models of acquired podocyte diseases ????Am J Physiol Renal Physiol http://www.kidney.de/pget.php?&tw=1&pmid=18784259 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=18784259 #FOAvip English Wikipedia <ref>{{Cite pmid|18784259}}</ref> Inducible rodent models of acquired podocyte diseases #MMPMID18784259 Pippin JW; Brinkkoetter PT; Cormack-Aboud FC; Durvasula RV; Hauser PV; Kowalewska J; Krofft RD; Logar CM; Marshall CB; Ohse T; Shankland SJ Am J Physiol Renal Physiol 2009[Feb]; 296 (2): F213-29 PMID18784259show ga Glomerular diseases remain the leading cause of chronic and end-stage kidney disease. Significant advances in our understanding of human glomerular diseases have been enabled by the development and better characterization of animal models. Diseases of the glomerular epithelial cells (podocytes) account for the majority of proteinuric diseases. Rodents have been extensively used experimentally to better define mechanisms of disease induction and progression, as well as to identify potential targets and therapies. The development of podocyte-specific genetically modified mice has energized the research field to better understand which animal models are appropriate to study acquired podocyte diseases. In this review we discuss inducible experimental models of acquired nondiabetic podocyte diseases in rodents, namely, passive Heymann nephritis, puromycin aminonucleoside nephrosis, adriamycin nephrosis, liopolysaccharide, crescentic glomerulonephritis, and protein overload nephropathy models. Details are given on the model backgrounds, how to induce each model, the interpretations of the data, and the benefits and shortcomings of each. Genetic rodent models of podocyte injury are excluded. |*Disease Models, Animal[MESH] |Animals[MESH] |Kidney Diseases/*pathology[MESH] |Mice[MESH] |Podocytes/*pathology[MESH]Inducible rodent models of acquired podocyte diseases (epmc).pdf DeepDyve Pubget Overpricing