Project: METAINFLAMMATION,CHRONIC DISEASES & CANCER (METACODEC)
Modulation of metabolic fluxes (cholesterol, fatty acid, glucose and glutamine) contributes to metainflammation (i.e, monocyte counts and/or macrophage efferocytosis) and chronic inflammatory diseases such as cardiometabolic diseases, these pathways most likely represent the tip of the iceberg. Indeed, myeloid cells encounter a substantial amount of other lipids and nutrients after ingesting atherogenic lipoprotein particles or clearing apoptotic cells. On the other side, the liver is often considered the primary organ of detoxification and when perturbed can lead to metabolic dysfunction. Together, this increases metabolic load, which will most likely impact myeloid behavior. Understanding the metabolic pathways that control this phenotypic switch in vivo will enable ground-breaking insights into novel mechanisms at the origin of the low-grade inflammation in the MetS and cancer and could give rise to innovative and tailored strategies to fight these diseases.