Psychological stress, vascular inflammation, and atherogenesis: potential roles of circulating cytokines

Area of Science:

• Cardiovascular Science
• Immunology
• Stress Physiology

Background:

• Cardiovascular disease remains a leading global cause of death.
• Chronic psychosocial stress is a known risk factor for atherosclerotic cardiovascular disease.
• The precise mechanisms linking stress to atherosclerosis are not fully elucidated.

Purpose of the Study:

• To review animal study evidence on stress-induced atherogenesis.
• To explore the role of proinflammatory cytokines in stress-related vascular inflammation.
• To propose cytokines as potential causal mediators and therapeutic targets.

Main Methods:

• Review of existing animal studies on stress and atherosclerosis.
• Analysis of mechanisms involving vascular inflammation and cytokine elevation.
• Synthesis of evidence linking circulating cytokines to stress-triggered atherogenesis.

Main Results:

• Animal studies suggest stress promotes atherogenesis by increasing vascular inflammation.
• Elevated circulating proinflammatory cytokines, such as tumor necrosis factor α and interleukin 6, are implicated.
• Circulating cytokines may causally mediate stress-induced vascular inflammation and atherosclerosis.

Conclusions:

• Stress may promote atherosclerosis by enhancing vascular inflammation through elevated proinflammatory cytokines.
• These cytokines, while biomarkers, may play a direct role in the disease process.
• Targeting circulating cytokines could be a strategy to counteract the adverse cardiovascular effects of chronic stress.