Emerging studies have revealed the crucial role of metabolic reprogramming in macrophage activation, which is known as immunometabolism 
. For example, in amino acid metabolism, arginine is converted to NO by iNOS in M1 macrophage, but metabolized by arginase-1 in M2 macrophage 
. M1 macrophage shows enhanced glycolytic metabolism and impaired mitochondrial oxidative phosphorylation (OXPHOS) 
. In addition, the ATP produced in M1 cells via glycolytic metabolism feeds the pentose phosphate pathway (PPP) 
. Fatty acid synthesis (FAS) organizes the plasma membranes under different inflammatory responses to regulate the inflammatory signaling, adhesion, and migration of macrophages 
. Fatty acid oxidation (FAO) is needed for NLRP3 inflammasome activation 
. These studies highlight the view that macrophagic metabolism status is tightly associated with macrophage functions.
Autophagy is an important part of cellular metabolism system that can be activated to supply materials and energy during nutrient deficiency. Therefore, the relationship between autophagy, metabolism, and macrophage function is a hotspot being noticed and investigated. In 2018, the “Autophagy, Inflammation, and Metabolism” (AIM) Center at the University of New Mexico has been established to specifically study this topic (ref: Autophagy, Inflammation, and Metabolism (AIM) Center of Biomedical Research Excellence). Further, mTOR functions as a key homeostatic regulator in nutrient signals and metabolic processes for cell growth 
, and its inhibition induce autophagy. As mentioned in the previous part, the mTOR pathway also regulates macrophage inflammatory pathway and polarization, which could be a possible link between cellular metabolism and macrophage function. AMP-activated protein kinase (AMPK) is a main sensor of cellular energy status and maintain metabolic balance 
. AMPK can control cell growth by inhibiting mTOR pathway via phosphorylation of TSC2 or RAPTOR 
. Therefore, AMPK can be involved into autophagy indirectly through acting on mTOR pathway. In addition, AMPK can also phosphorylate ULK1 complex directly to activate autophagy 
. According to previous studies, AMPK is regarded as a suppressor of inflammation in immune cells including macrophage 
, indicating a potential connection among autophagy, cellular metabolism and macrophage inflammation. Besides, growing evidence has revealed that autophagy can regulate immune cell differentiation by alteration of metabolic states in immune cells 
. Collectively, upon mTOR activation, immune cells show decreased autophagy, but increased cellular glycolytic and pro-inflammatory response. However, AMPK induction induce autophagy, increase cellular OXPHOS and anti-inflammatory response 
. Moreover, increased lipophagy (autophagic target on lipid specifically) has been proved to accelerate macrophage cholesterol efflux so that to reduce macrophage foam cells in atherosclerosis 
. Although lots of evidence is being uncovered, the regulation network between autophagy, metabolism, and macrophage function has not been well understood. The key metabolic products that link macrophage function and autophagy would be an interesting topic to explore.