Biomolecular basis of the role of chronic psychological stress in the development and progression of Atherosclerosis

Abstract

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.