Yao BC, et al. J Int Med Res. 2019 Apr;47(4):1429-1440.
Yao BC, et al., conducted a review study to present a summary of the impact of chronic stress on the pathophysiological mechanism of Atherosclerosis (AS).
Chronic stress effects on inflammation
Inflammation is a pathological process represented by injury or tissues breakdown triggered by a various cytological and chemical reactions. Pain, heat, redness, swelling and loss of function are the ordinary signs of inflammation, which is linked to chronic stress. Although, in the pathological process of AS, during chronic stress, inflammation plays a vital role. It is widely known that chronic stress can lower hypothalamic–pituitary–adrenal axis activity and activate the sympathetic adrenal medulla which increases production of inflammatory cytokines.
VCAM-1 is a member of the immunoglobulin gene superfamily which is particularly demonstrated in vascular endothelial cells, and its ligands are a4b1 (VLA-4) and a4b7. Its correlation with VLA-4 is involved in the inflammation which is triggered by leukocytes and enhances the pathological process of AS.
Chronic stress effects on lipid metabolism
Lipid metabolism defines as the physiological procedure of biosynthesis (anabolism) and degradation (catabolism) of lipids.
Additionally, there is data-based evidence that stress-induced hyperlipidaemia and enhances oxidative stress are firmly linked to AS. Partially, chronic social stress induces obesity by means of excessive accumulation of fat, and various studies found that obesity can elevate the occurrence of cerebrovascular diseases. Hence, adequately weight loss is advantageous for AS.
Chronic stress effects on hormones
A hormone can be known as a chemical content that has a particular regulatory effect on the activity of a specific organ or organs. Corticosterone is an anti-inflammatory hormone which can deteriorate AS in arteries, a method that is correlated with enhanced dyslipidemia. However, one study found that the quantity of norepinephrine elevated in a chronic stress experimental group. Hence, these hormones can be a unique objective for the treatment and prevention of cardiovascular and cerebrovascular diseases.
Chronic stress effects on macrophages
Various research studies have demonstrated that the expression of cytokines developed mostly by stress-catecholamine macrophages elevates by chronic mental stress. During stress, catecholamines attach to β-adrenal receptors on the macrophage surface, which provokes the expression of cytokines such as C-reactive protein, interleukin-1, interleukin-6 and tumour necrosis factor, which are all linked to AS.
Thus, the mechanism of chronic stress on AS should be further examined to offer a theoretical basis for efforts to exclude the impact of chronic stress on the cardio-cerebral vascular system. Moreover to positive control of risk factors, study data provides that lowering chronic stress can effectively reduce stroke incidence.
