Abstract: Myeloid-derived suppressor cells (MDSCs) are bone marrow-derived immature cells with heterogeneity and immunosuppressive activity. They often originate from common myeloid progenitors in pathological conditions such as inflammation, infection, and tumor, and play an important role in tumor immunity. In tumor microenvironment, glucose metabolism occurs mainly through aerobic glycolysis. Hence, the reprogramming of glucose metabolism will enhance the immunosuppressive activity of MDSCs, inhibiting the proliferation and function of effector T cells. Existing research mainly involves the regulation of glucose metabolism of MDSCs by using AMP-activated protein kinase (AMPK) as the upstream regulator to regulate downstream genes through multiple signal pathways. This study summarizes the glycolysis-related signaling pathways and their effects on the function of MDSCs.