Acute psychological stress accelerates the progression of atherosclerosis

• Applicant: Professor Dr. Hendrik Sager
• Subject Area: Cardiology, Angiology
• Term: from 2017 to 2020
• Project identifier: Deutsche Forschungsgemeinschaft (DFG) - Project number 383698746

We have known for decades that psychosocial stress is an independent risk factor for atherosclerosis. Within hours after onset acute psychosocial stress associates with a high incidence of cardiovascular events that are caused by plaque progression and destabilization with rupture. The mechanisms for this rapid aggravation remain largely unknown. Inflammatory plaque leukocytes are main instigators of plaque progression and destabilization. We hypothesize that acute psychosocial stress leads to a rapid expansion of pro-inflammatory leukocytes within atherosclerotic plaques rendering them more vulnerable and prone to rupture. Leukocytes are deployed to the plaque by the leukocyte supply chain: Leukocytes are released from bone marrow or spleen into the blood, recruited to the plaque, and can self-expand locally by in-situ proliferation.In this proposal we aim1) to study whether acute psychosocial stress influences the leukocyte supply chain (phenotype).2) to investigate the mechanisms how stress affects the leukocyte supply chain (mechanism).3) to test how our findings translate to humans (translation).Our research will gain new insight into how psychosocial stress modifies the aggravation of atherosclerosis and may reveal new therapeutic avenues for inhibiting atherosclerotic disease progression.

• DFG Programme: Research Grants