Alteration of the monocyte repertoire after myocardial infarction – novel mechanistic insights and therapeutic avenues

Project start
Institution: Deutsches Herzzentrum München
Applicant: Prof. Dr. med. Hendrik Sager
EKFS funding line: Else Kröner-Exzellenzstipendium
Identification of human blood monocytes

Myocardial infarction (MI) is a major contributor to worldwide morbidity and mortality. MI occurs after atherosclerotic plaque rupture/erosion leading to atherothrombosis which in turn blocks supply of oxygenated blood to areas of the heart. Consequently, parts of the heart muscle become hypoxic and die off. This triggers a systemic inflammatory reaction which leads to an accumulation of inflammatory cells in the infarct area. These blood-derived immune cells exert different function during the course of MI. Early after MI, they remove debris and dead cells, while during a later stage they aid to replace damaged tissue with stable scar tissue, which does not anymore contribute to cardiac contraction. The reservoirs for immune cells shrink rapidly due to hearts’ high demand of these cells. The bone marrow responds to MI and transiently elevates production of these cells. In this project, we investigate whether the bone marrow also supplies qualitatively different cells apart from the known quantitive alterations. Our studies will help to better understand the inflammatory networks that are established after MI and to test them as novel therapeutic targets. Specifically, we aim to beneficially modulate scar formation after MI to lower that the incidence of heart failure and malignant arrhythmias to ultimately lower infarct-associated mortality and morbidity.

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