Chronic stress refers to the non-specific systemic reaction that occurs when the body is stimulated by various internal and external negative factors over a long time. The physiological response to chronic stress exposure has long been recognized as a potent modulator in the occurrence of atherosclerosis. Furthermore, research has confirmed the correlation between atherosclerosis and cardiovascular events. Chronic stress is pervasive during negative life events and may lead to the formation of plaque. Several epidemiological studies have shown that chronic stress is an independent risk factor for the development of vascular disease and for increased morbidity and mortality in patients with pre-existing coronary artery disease. One possible mechanism for this process is that chronic stress causes endothelial injury, directly activating macrophages, promoting foam cell formation and generating the formation of atherosclerotic plaque. This mechanism involves numerous variables, including inflammation, signal pathways, lipid metabolism and endothelial function. The mechanism of chronic stress in atherosclerosis should be further investigated to provide a theoretical basis for efforts to eliminate the effect of chronic stress on the cardiocerebral vascular system.

The prevalence of overweight–obesity has increased sharply among undergraduates worldwide. In 2016, approximately 52% of adults were overweight–obese. This cross-sectional study aimed to investigate the prevalence of overweight–obesity and explore in depth the connection between eating habits and overweight–obesity among Chinese undergraduates. The study population included 536 undergraduates recruited in Shijiazhuang, China, in 2017. They were administered questionnaires for assessing demographic and daily lifestyle characteristics, including sex, region, eating speed, number of meals per day, and sweetmeat habit. Anthropometric status was assessed by calculating the body mass index (BMI). The determinants of overweight–obesity were investigated by the Pearson χ 2 test, Spearman rho test, multivariable linear regression, univariate/multivariate logistic regression, and receiver operating characteristic curve analysis. The prevalence of undergraduate overweight–obesity was 13.6%. Sex [male vs female, odds ratio (OR): 1.903; 95% confidence interval (95% CI): 1.147–3.156], region (urban vs rural, OR: 1.953; 95% CI: 1.178–3.240), number of meals per day (3 vs 2, OR: 0.290; 95% CI: 0.137–0.612), and sweetmeat habit (every day vs never, OR: 4.167; 95% CI: 1.090–15.933) were significantly associated with overweight–obesity. Eating very fast was positively associated with overweight–obesity and showed the highest OR (vs very slow/slow, OR: 5.486; 95% CI: 1.622–18.553). However, the results of multivariate logistic regression analysis indicated that only higher eating speed is a significant independent risk factor for overweight/obesity (OR: 17.392; 95% CI, 1.614–187.363; P = .019). Score meng = 1.402 × score sex + 1.269 × score region + 19.004 × score eatin speed + 2.546 × score number of meals per day + 1.626 × score sweetmeat habit and BMI = 0.253 × Score meng + 18.592. These 2 formulas can help estimate the weight status of undergraduates and predict whether they will be overweight or obese.

Atherosclerosis (AS) is a chronic vascular inflammatory disease, in which the lipid accumulation in the intima of the arteries shows yellow atheromatous appearance, which is the pathological basis of many diseases, such as coronary artery disease, peripheral artery disease and cerebrovascular disease. In recent years, it has become the main cause of death in the global aging society, which seriously endangers human health. As a result, research on AS is increasing. Lesions of atherosclerosis contain macrophages, T cells and other cells of the immune response, together with cholesterol that infiltrates from the blood. Recent studies have shown that chronic stress plays an important role in the occurrence and development of AS. From the etiology of disease, social, environmental and genetic factors jointly determine the occurrence of disease. Atherosclerotic cardio-cerebrovascular disease (ASCVD) is often caused by chronic stress (CS). If it cannot be effectively prevented, there will be biological changes in the body environment successively, and then the morphological changes of the corresponding organs. If the patient has a genetic predisposition and a combination of environmental factors triggers the pathogenesis, then chronic stress can eventually lead to AS. Therefore, this paper discusses the influence of chronic stress on AS in the aspects of inflammation, lipid metabolism, endothelial dysfunction, hemodynamics and blood pressure, plaque stability, autophagy, ferroptosis, and cholesterol efflux.

Objective: Chronic stress may lead to augmented incidence rates of coronary and cerebrovascular diseases associated with atherosclerosis. However, few studies have focused on the effect of chronic stress on atherosclerosis plaque formation. Therefore, this study was designed to directly evaluate how chronic stress affects atherosclerosis. Methods: Thirty rabbits were divided into three groups: the control group, balloon-injury operation þ high-fat diet model group, and chronic stress þ balloon-injury operation þ high-fat diet model group. Physical and social stress were induced, and proteomic methods were applied to identify specific markers. Results: After protein determination, the chronic stress þ balloon-injury operation þ high-fat diet model group exhibited significant upregulation of the following apoptosis-related proteins: UBE2K, caspase 3, caspase 9, BAX, P53, and FAS. In particular, real-time polymerase chain reaction showed that the protein expression of caspase 9 was significantly downregulated in the stress group compared with the non-stress groups. However, the other proteins showed significantly increased expression in the stress group. Conclusion: Chronic stress may promote cell apoptosis in the physiopathologic process of atherosclerosis.

Objective To use bioinformatics tools to screen for gene biomarkers from monocytes, which play an important role in the pathogenesis of atherosclerosis. Methods Two expression profiling datasets (GSE27034 and GSE10195) were obtained from the Gene Expression Omnibus dataset and the differentially expressed genes (DEGs) between atherosclerotic human peripheral blood mononuclear cells (PBMC) samples and control subjects were screened using GEO2R. Gene Ontology and Kyoto Encyclopedia of Genes and Genomes pathway enrichment analyses were conducted for the DEGs. STRING and MCODE plug-in of Cytoscape were used for constructing a protein–protein interaction network and analysing hub genes. Results The two datasets had 237 DEGs in common between non-atherosclerotic- and atherosclerotic PBMC samples. Functional annotation demonstrated that these DEGs were mainly enriched in protein binding, positive regulation of transcription from RNA polymerase II promoter, nucleus and viral carcinogenesis. Five hub genes, FBXL4, UBOX5, KBTBD6, FZR1 and FBXO2, were identified. Conclusion This present bioinformatics analysis identified that the FBXL4, UBOX5, KBTBD6 and FBXO21 genes might play vital roles in the pathogenesis of atherosclerosis. These four genes might represent new biomarkers for the diagnosis and treatment of atherosclerosis.