Myeloid Cell Diversity and Impact of Metabolic Cues during Atherosclerosis

Abstract

Myeloid cells are key contributors to tissue, immune and metabolic homeostasis and their alteration fuels inflammation and associated disorders such as atherosclerosis. Conversely, in a classical chicken-andegg situation, systemic and local metabolism, together with receptormediated activation, regulate intracellular metabolism and reprogram myeloid cell functions. Those regulatory loops are notable during the development of atherosclerotic lesions. Therefore, understanding the intricate metabolic mechanisms regulating myeloid cell biology could lead to innovative approaches to prevent and treat cardiovascular diseases. In this review, we will attempt to summarize the different metabolic factors regulating myeloid cell homeostasis and contribution to atherosclerosis, the most frequent cardiovascular disease.

Metabolic regulation of macrophage proliferation and function in atherosclerosis

“…Under inflammatory conditions, macrophages shift their metabolism toward glycolysis and away from oxidative phosphorylation [37,38]. To meet the increased demand for glucose, macrophages upregulate the glucose transporter GLUT1c [39].…”