| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 2082057 | Drug Discovery Today: Disease Models | 2014 | 7 Pages |
Abstract
Experiments in genetically engineered mice have elucidated the key role of the complement system in the pathogenesis of several renal disorders. This has led to the clinical evaluation of agents that inhibit complement activation in patients with complement-mediated kidney disease. Here we discuss the mouse models of lupus nephritis, C3 glomerulopathy and atypical hemolytic uremic syndrome, together with an inducible model of antiphospholipid syndrome. Evidence for and against therapeutic modulation of specific complement pathways in these disorders is presented.
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Authors
Thomas D. Barbour, Matthew C. Pickering, H. Terence Cook,