Cardiovascular diseases are the leading cause of death worldwide. Pathophysiologically, metabolic and inflammatory processes contribute substantially to the development and progression of cardiovascular diseases. Over the past decade, the role of disease-propagating inflammatory processes has been strengthened and reframed, leading to trials testing anti-inflammatory drugs for the treatment of atherosclerosis and its complications. Despite these achievements, further research in both pre-clinical and clinical studies is warranted to explore new targets, to better identify responders, and to refine therapy strategies to combat inflammation in human disease. Environmental disturbances, so-called lifestyle-associated cardiovascular risk factors, greatly alter the immune system in general and leukocytes in particular, thus affecting the progression of atherosclerosis. Epidemiological studies have shown that exposure to mental stress can be closely linked to the occurrence of cardiovascular disease. Here, we describe how acute and chronic mental stress alter the immune system via neuroimmune interactions, thereby modifying vascular inflammation. In addition, we identify gaps that still need to be addressed in the future.
Keyphrases
- cardiovascular disease
- cardiovascular risk factors
- oxidative stress
- mental health
- cardiovascular events
- anti inflammatory drugs
- type diabetes
- endothelial cells
- stress induced
- metabolic syndrome
- liver failure
- risk factors
- physical activity
- coronary artery disease
- bone marrow
- combination therapy
- acute respiratory distress syndrome
- hepatitis b virus
- replacement therapy
- pluripotent stem cells
- case control