The more critical murderer of atherosclerosis than lipid metabolism: chronic stress

Abstract

BackgroundThe mortality of atherosclerotic cerebrovascular disease is on the rise, and changes in intimal and media thickness are a leading cause of cerebral ischemia-related death. Levels of low density lipoprotein cholesterol (LDLC), total cholesterol (TC), and chronic stress (CS) are all recognized risk factors for atherosclerosis (AS). However, the leading independent risk factor is indistinct. This study explored the effects of chronic stress, LDLC, and TC on AS and intimal and media thickness, preliminarily explored the main risk factor of AS, and analyzed the related histocyte mechanisms for macrophages and endothelial cells.MethodsConditions include normal, high-fat diet (HF), and HF plus CS. The correlations between intimal and media thickness and general risk factors were analyzed using χ2, Spearman’s rho test, and multiple linear regression. Univariate Cox regression was used to identify potential factors that affect the non-depression time (NDT). We performed a ROC curve to determine the ability of this condition to predict the thickness. Immunohistochemistry was implemented to detect macrophagocytes and endotheliocytes.ResultsBased on χ2 and Spearman’s rho test, LDLC, TC, and CS are all related with intimal and media thickness (P < 0.05). However, in multiple linear regression, CS is still a risk factor of thickness (P < 0.05) but LDLC and TC are not. High levels of LDLC, TC, and CS were correlated with poor NDT (P < 0.05). This condition can predict the thickness sensitively. The endarterium is richest in macrophagocytes, and the arrangement of endotheliocytes is disordered and cracked under CS.ConclusionCS is the main independent risk factor for AS and intimal (and media) thickness, rather than LDLC or TC.

Comparison of Mortality and Comorbidity Rates Between Holocaust Survivors and Individuals in the General Population in Israel

“…For example, chronic stress has been shown to be associated with increased mortality risk among patients with atherosclerosis. 12 It is conceivable that the stress response among Holocaust survivors is different so that these survivors are less sensitive to the consequences of some comorbidities. It has been shown that soldiers who have experienced combat-related trauma find greater meaning and satisfaction in their later lives secondary to these traumatic experiences.…”

Citrate Synthase and OGDH as Potential Biomarkers of Atherosclerosis under Chronic Stress

“…The increase in inflammatory cytokines and the expression of adhesion molecules through certain pathways can induce monocyte accumulation and lymphocyte adhesion [ 28 ]. In addition, CS leads to an imbalance in lipid metabolism, affects epigenetic patterns, induces depression, directly activates macrophages, promotes foam cell formation, and induces the formation of atherosclerotic plaques [ 29 ]. Through epidemiological investigations and laboratory studies, it has been found that stress load has become one of the most important factors in the development of AS in modern society [ 15 ].…”

Red-Osier Dogwood Extracts Prevent Inflammatory Responses in Caco-2 Cells and a Caco-2 BBe1/EA.hy926 Cell Co-Culture Model

“…These results are consistent with one previous study [30], in which 1 ng/mL TNF-α induced secretions of IL-8, monocyte chemoattractant protein-1 (MCP-1), vascular endothelial growth factor (VEGF), and ICAM-1 in EA.hy926 cells. Clinical evidence has shown that disorders of lipid metabolism are associated with the pathogenesis of atherosclerosis [31,32]. An oxidized form of LDL (ox-LDL) has been reported to disturb redox balance and trigger the NF-κB mediated inflammation [33,34].…”