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Inflammation is a hallmark of many aspects of cardiovascular disease. In atherosclerosis inflammation correlates with plaque progression, severity and stability. The abundance of inflammatory cells, and more specifically macrophages often as lipid laden foam cells, associates with key features of plaque instability and circulating inflammatory markers are good predictors of clinical disease outcome.

In my group we study the molecular regulation of macrophages, and their precursors monocytes, in cardiovascular disease, with a specific focus on atherosclerosis. We investigate regulation of macrophage subtypes, ranging from disease promoting pro-inflammatory macrophages to cells with an anti-inflammatory phenotype that can dampen atherosclerosis progression and stabilize plaques. We are using a unique approach of cellular murine and human monocyte and macrophage tools combined with state-of-the-art mouse models and cells and tissue samples from cardiovascular disease patients to cover the complete axis from fundamental mechanistic work to translational studies.

The work in my group is currently particularly focusing on the following aspects of monocyte and macrophage regulation in cardiovascular disease:

1) Epigenetic processes that control monocytes and macrophages in disease
2) Cellular energy metabolism as a target to regulate cellular phenotype
3) Cytokines and signaling pathways that control monocytes and macrophages
4) Consequences of dyslipidemia for cellular function

With our studies we aim to identify the mechanisms that underlie the dysfunctioning of monocytes and macrophages in cardiovascular disease to better understand disease development, identify markers and makers of disease and to find new approaches for diagnosis and treatment.

Macrophages, monocytes, innate immunity, epigenetics, atherosclerosis, immunometabolism, cytokines