Abstract

Bipradas Roy* and Mahbub E Sobhani

Psychological stress has extreme adverse consequences on health. However, the molecular mechanisms that mediate and accelerate the process of atherosclerosis due to stress hormone are not well defined. This review has focused on diverse molecular paths that come out in response to chronic psychological stress via the release of excessive glucocorticoids (GCs), involved in the progression of atherosclerosis. GCs acts as a pathological agent of insulin resistance (IR), inhibition of NO and prostacyclin synthesis, over synthesis of reactive oxygen species (ROS) and Angiotensin-II (AT-II). All these processes may induce changes in blood pressure through different mechanisms. In one side high blood pressure may disrupts the arterial endothelial cells and on the other side IR triggers the increased production of very low density lipoprotein (LDL). LDL penetrates through the disrupted endothelial linings into the sub-endothelial space and converts into oxidized LDL (Ox-LDL).Ox-LDL binds to the arterial endothelial cells and signals for the expression of vascular cell adhesion molecules and other peptides. Circulatory monocytes bind to the vascular cell adhesion molecules and penetrate through the endothelial layer and convert into macrophage within the sub endothelial space. Macrophages and some vascular smooth muscle cells (VSMC) in the medial layer engulf the Ox-LDL and convert into foam cells. VSMC also migrate from the medial layer and arrange around the dead necrotic core of the foam cells to form a fibrous cap as well as atherosclerotic plaque.