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The goal of this study was to examine the role of endoplasmic reticulum (ER) stress signaling and the contribution of glycogen synthase kinase (GSK)-3β activation in hyperglycemic, hyperhomocysteinemic, and high-fat-fed apolipoprotein E-deficient (apoE(-/-)) mouse models of accelerated atherosclerosis.

Endoplasmic Reticulum Stress and Glycogen Synthase Kinase-3β Activation in Apolipoprotein E–Deficient Mouse Models of Accelerated Atherosclerosis