Mouse models of diabetic nephropathy.

By M. Breyer, E. Böttinger, F. Brosius, T. Coffman, Raymond C. Harris, C. Heilig, K. Sharma. Journal of the American Society of Nephrology, 2005

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Mechanisms of diabetic complications. (2013, methodology): “These models, however, do not progress to more advanced renal disease seen in humans which is characterized by a loss of glomerular filtration, overt proteinuria, and advanced structural lesions (22, 61).”
Streptozotocin‐Induced Diabetic Models in Mice and Rats (2015, background): “, 2007), diabetic nephropathy (Breyer et al., 2005), and diabetic atherosclerosis (Wu and Huan, 2007).”
Glucose-induced reactive oxygen species cause apoptosis of podocytes and podocyte depletion at the onset of diabetic nephropathy. (2006, methodology): “To determine whether diabetes induces podocyte depletion and to delineate a temporal relationship between onset of diabetes, albuminuria, and changes of podocyte numbers, we subjected two genetic models of experimental diabetes, including Akita (type 1 diabetes) (26,27) and db/db (type 2 diabetic) m”
Molecular mechanisms of diabetic kidney disease. (2014, neutral): “Most mouse models of DKD are limited, as mice do not exhibit a progressive renal function decline (14).”
Macrophage Dysfunction Impairs Resolution of Inflammation in the Wounds of Diabetic Mice (2010, background): “From a metabolic and related mechanistic stand-point, NOD and db/db diabetic mice have several fundamental differences [22,30,37].”