In vivo inhibition of nuclear factor of activated T-cells leads to atherosclerotic plaque regression in IGF-II/LDLR^-/-ApoB^100/100 mice.

ABSTRACT:

Aims

Despite vast clinical experience linking diabetes and atherosclerosis, the molecular mechanisms leading to accelerated vascular damage are still unclear. Here, we investigated the effects of nuclear factor of activated T-cells inhibition on plaque burden in a novel mouse model of type 2 diabetes that better replicates human disease.

Methods & results

IGF-II/LDLR^-/-ApoB^100/100 mice were generated by crossbreeding low-density lipoprotein receptor-deficient mice that synthesize only apolipoprotein B100 (LDLR^-/-ApoB^100/100) with transgenic mice overexpressing insulin-like growth factor-II in pancreatic β cells. Mice have mild hyperglycaemia and hyperinsulinaemia and develop complex atherosclerotic lesions. In vivo treatment with t

SUBMITTER: Blanco F 

PROVIDER: S-EPMC6039864 | biostudies-literature | 2018 Jul

REPOSITORIES: biostudies-literature