Epigenetic regulation of macrophage function

Atherosclerosis is a lipid-driven chronic inflammatory disorder with a key role for macrophages in all disease stages. Macrophages are involved as scavengers of lipids, regulate inflammation, attract other immune cells and contribute to the resolution of inflammation, fibrosis and plaque stability. In this thesis, I investigate the potential for intervening at the level of transcriptional and epigenetic regulation to manipulate macrophages to dampen inflammation and to combat atherosclerosis. I conclude that macrophage function is tightly regulated by epigenetic processes and postulate that specific targeting of epigenetic enzymes or processes in innate immune cells, like macrophages, should be considered as future therapeutic opportunity in disease.