Cardiovascular disease is a major cause of morbidity and mortality worldwide. Epidemiological studies have clearly demonstrated that chronic psychosocial stress increases the risk of atherosclerotic cardiovascular disease and this may involve multiple mediators and regulating pathways, whereas the precise mechanisms underlying the effects of stress on development of atherosclerosis are not completely understood. In this mini review, we summarize current information from various animal studies suggesting that stress may promote atherogenesis by stimulating vascular inflammation via elevating the level of circulating proinflammatory cytokines (such as tumor necrosis factor α and interleukin 6). Although circulating cytokines can serve as reliable biomarkers of systemic inflammation, in light of the emerging evidence, we propose that these molecules may also have a causal role in mediating stress-triggered vascular inflammatory reaction and atherogenesis. Further studies are warranted to clarify whether targeting circulating cytokines may be an effective approach to reduce the detrimental effects of chronic stress.