Myeloid cell metabolic pathways

Myeloid cell metabolic pathways refer to the integrated network of biochemical reactions, including glycolysis, the tricarboxylic acid (TCA) cycle, oxidative phosphorylation, and amino acid metabolism, that govern the activation and effector functions of myeloid lineage cells such as macrophages, dendritic cells, and myeloid-derived suppressor cells (MDSCs) [1][3]. In various disease states, particularly cancer, these cells undergo metabolic reprogramming; for instance, MDSCs and tumor-associated macrophages (TAMs) often utilize increased glycolysis and amino acid catabolism (via enzymes like IDO1 and Arginase 1) to create an immunosuppressive environment that facilitates tumor escape [2][4]. Targeting these pathways involves using small molecules to inhibit metabolic checkpoints, thereby 're-educating' the myeloid compartment to restore anti-tumor immunity or dampen pathological inflammation [5]. This approach is a cornerstone of the emerging field of immunometabolism, offering synergistic potential when combined with traditional immune checkpoint inhibitors [3][6]. Sources: [1] Nature Reviews Cancer (2017) 17:239-253; [2] Cell Metabolism (2019) 30(6):1028-1044; [3] Journal for ImmunoTherapy of Cancer (2020) 8:e000853; [4] Frontiers in Oncology (2021) 11:638385; [5] Science (2019) 366(6466):eaar5112; [6] Trends in Immunology (2018) 39(2):132-147.

Other names

Myeloid immunometabolismMetabolic reprogramming of myeloid cellsMyeloid cell metabolismMonocyte and macrophage metabolic pathways

Modulation of metabolic flux through the inhibition of specific enzymes (e.g., IDO1, Arginase 1, LDHA) or transporters (e.g., GLUT1, MCT1) to alter the functional phenotype of myeloid cells, typically shifting them from an immunosuppressive (M2-like) to a pro-inflammatory (M1-like) state in oncology, or vice versa in inflammatory diseases [1][2].