| First Author | Pippin JW | Year | 2009 |
| Journal | Am J Physiol Renal Physiol | Volume | 296 |
| Issue | 2 | Pages | F213-29 |
| PubMed ID | 18784259 | Mgi Jnum | J:144605 |
| Mgi Id | MGI:3831264 | Doi | 10.1152/ajprenal.90421.2008 |
| Citation | Pippin JW, et al. (2009) Inducible rodent models of acquired podocyte diseases. Am J Physiol Renal Physiol 296(2):F213-29 |
| abstractText | 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. |
