Harry Björkbacka

Focal accumulation of immune cells and lipids in the vascular wall leads to the formation of atherosclerotic plaques. Plaques occasionally erode or rupture, causing the blood to clot and restrict blood flow, with serious clinical consequences such as acute myocardial infarctions and strokes. Even though our understanding of the disease mechanisms underlying atherosclerosis has advanced substantially in recent years, identification and treatment of vulnerable atherosclerotic plaques remains a considerable challenge. Consequently, atherosclerotic cardiovascular disease is still the leading cause of death worldwide and the burden on society caused by cardiovascular disease will likely increase dramatically with the daunting rise of diabetes and its associated cardiovascular complications. Although lipid-lowering drugs have revolutionized treatment of cardiovascular disease, this treatment only reduces the cardiovascular risk by about 25-50%. Thus, therapies targeting other disease mechanisms, such as inflammation, are needed to minimize the remaining considerable risk.

It is today known that cellular metabolism and immune responses are tightly intertwined. For instance, activated leukocytes reprogram their metabolism to meet the demands needed to perform their immune functions efficiently. Our research aims to understand how immune cells reprogram their metabolism to sustain plaque inflammation and promote atherosclerosis development, and explore if targeting the reprogrammed cellular metabolism could be a conceptually novel approach to limit plaque inflammation and atherosclerosis development.

Course coordinator for the bachelor thesis in biomedicine course (BIMK90). Member of the Examination Committe appointed by the Master's Programmes Board tasked with helping course coordinators to improve examination and assessments procedures.