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Published on: December 2, 2015
Pathophysiological mechanisms linking depression and atherosclerosis: an overview
Insights
Depression is linked to cardiovascular events through complex pathways. Key factors include the autonomic nervous system and inflammation, contributing to atherosclerosis and heart disease.
Area of Science:
- Cardiovascular Science
- Psychiatry
- Pathophysiology
Background:
- Depression is independently associated with increased cardiovascular events.
- Pathophysiological links between depression and coronary heart disease are not fully understood.
- Traditional cardiovascular risk factors alone do not explain this association.
Discussion:
- Autonomic nervous system (ANS) dysfunction, low-grade inflammation, platelet activation, hypothalamic-pituitary-adrenal (HPA) axis dysregulation, and genetic factors contribute to endothelial dysfunction.
- These factors promote atherosclerosis, plaque rupture, and thrombosis.
- Depression-related dysfunctions in the ANS and HPA axis appear central, driving chronic inflammation and endothelial damage.
Key Insights:
- The interplay of ANS and HPA axis dysfunction in depression significantly promotes chronic inflammation.
- Endothelial dysfunction and platelet activation are critical steps in atherosclerosis development linked to depression.
- Multiple interrelated pathophysiological mechanisms link depression to cardiovascular disease.
Outlook:
- Further research into the interconnectedness of these mechanisms is crucial.
- Targeting ANS and HPA axis dysregulation may offer novel therapeutic strategies for cardiovascular risk in depressed patients.
- Understanding these pathways can lead to integrated treatment approaches for mental and cardiovascular health.
Abstract:
It is well recognized that depression is independently associated with cardiovascular events. However, uncertainties remain on the pathophysiological pathways underlying the association between depression and coronary heart disease. In addition to the traditional cardiovascular risk factors, autonomic nervous system (ANS), low grade of inflammation, platelet and hypothalamic-pituitary-adrenal axis function and genetic factors may adversely impact the endothelium of the arterial wall. We provide an overview of the pathophysiological mechanisms and indices which seem to have a role in promoting and accelerating atherosclerosis and its complications due to plaque rupture and thrombosis. Given that the relationship between depression and atherosclerosis cannot be fully explained by single mechanisms, which seem at least partially interrelated, the depression-related dysfunctions in the ANS and hypothalamic-pituitary-adrenal axis seem to play a major role, promoting chronic inflammation, endothelial dysfunction and platelet activation and aggregation, which in turn are key steps in the development of atherosclerosis and its complications.
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