Development and prevention of advanced diabetic nephropathy in RAGE-overexpressing mice.

ABSTRACT: Vascular complications arising from multiple environmental and genetic factors are responsible for many of the disabilities and short life expectancy associated with diabetes mellitus. Here we provide the first direct in vivo evidence that interactions between advanced glycation end products (AGEs; nonenzymatically glycosylated protein derivatives formed during prolonged hyperglycemic exposure) and their receptor, RAGE, lead to diabetic vascular derangement. We created transgenic mice that overexpress human RAGE in vascular cells and crossbred them with another transgenic line that develops insulin-dependent diabetes shortly after birth. The resultant double transgenic mice exhibited increased hemoglobin A(1c) and serum AGE levels, as did the diabetic controls. The double transgenic mice d

SUBMITTER: Yamamoto Y 

PROVIDER: S-EPMC203021 | biostudies-literature | 2001 Jul

REPOSITORIES: biostudies-literature