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Table 1 Metabolic pathways in macrophages

From: Metabolic reprogramming in macrophage responses

 

M1/M[LPS(±IFNγ)]

M2/M[IL-4/IL-10]

Contradictory observations

Arginine metabolism

Metabolized arginine to NO and citrulline by iNOS (9)

Hydrolyzed arginine to ornithine and urea by arginase (9)

 

Glycolysis

Glycolysis is enhanced (21)

Glycolysis is essential for M2 activation (11,34,36,37)

Glycolysis does not affect M2 activation (38)

PPP

Increased PPP pathway, providing NADPH for the production of ROS and NO (25,41)

Upregulation of CARKL, which is contributed to the suppression of PPP (41)

 

OXPHOS

Reduced OXPHOS (21) with the conditions of high mitochondrial membrane potential, M1 leads to reversal of the normal direction of electron flow causing RET at complex I, driving ROS production (56)

High OXPHOS (21,34)

 

TCA cycle

Broken in two places — after citrate and after succinate (40)

An intact TCA cycle (40)

 

FAS

FAS is increased and is contributed to the pro-inflammatory responses (60-62)

FAS fuels of FAO in M2 activation (37)

 

FAO

 

Enhanced FAO is contributed to the activation of M2 (65,66)

FAO is not essential during the M2 activation (67,69)

Glutamine metabolism

Glutamine can replesh succinate through “GABA shunt” and anaplerosis from a-ketoglutarate, and promotes the inflammatory response of macrophages (53)

Glutamine is contributed to the M2 activation (40,71)

Transiently deprived macrophage of glutamine has no effect for M1 polarization (40)