Fig. 1

Metabolites, metabolic pathways and related metabolic genes that play the roles in apoptosis. Deficiencies of various substances involved in metabolism affect the relevant metabolic pathways and apoptosis. Glycolysis can be inhibited in the presence of Glut1 deficiency, which promotes the development of apoptosis. ACLY, a key enzyme involved in the conversion of citric acid to oxaloacetate and acetyl CoA, works with ACC1, an important enzyme in the process of acetyl-CoA production, to regulate the content of α-KG and promote ETV4, which in turn promotes apoptosis. ROS usually promotes apoptosis. When TIGAR inhibits the important oxidative ROS, apoptosis can be suppressed. Gln deletion synergizes with GLS1 to promote ROS-related apoptosis. Inhibition of NAMPT prevents the conversion of saturated fatty acids to monounsaturated fatty acids and promotes apoptosis. The red boxes represent negative regulators and the green boxes represent positive regulators