Key result
Chronic psychosocial stress may promote atherogenesis by stimulating vascular inflammation via elevating circulating proinflammatory cytokines such as TNF-α and IL-6.
Why the study?
Does chronic psychosocial stress promote atherogenesis via vascular inflammation?
Does chronic psychosocial stress promote atherogenesis via vascular inflammation?
Chronic psychosocial stress may promote atherogenesis through elevated circulating proinflammatory cytokines, suggesting a potential therapeutic target for reducing stress-related cardiovascular risk.
May inform stress assessment in CVD prevention; leaves open whether cytokine targeting alters atherogenesis.
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.
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Lu et al. (2013) conducted a review in Atherosclerotic cardiovascular disease. Psychological stress was evaluated. Chronic psychosocial stress may promote atherogenesis by stimulating vascular inflammation via elevating circulating proinflammatory cytokines such as TNF-α and IL-6.
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