Abstract
Atherosclerosis is a major underlying cause of cardiovascular disease. Our lab and others have identified a role for endoplasmic reticulum (ER) stress in the dysregulation of lipid metabolism and the development of atherosclerosis, however the molecular mechanisms by which conditions of ER stress promote the pro-atherogenic processes are not understood. Recently, we have found that ER stress-inducing agents can activate glycogen synthase kinase (GSK)-3 α and β, homologous kinases involved in the regulation of cell metabolism.
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