Table 1.

Therapeutic targeting of macrophage metabolism for obesity and atherosclerosis

	Treatment	Metabolic change	Preclinical outcomes	Ref
Obesity	IL-4	Upregulates FAO and OXPHOS	Improved insulin sensitivity	(93)
	IL-33	Increases mitochondrial biogenesis	Prevention of HFD-induced insulin resistance	(135)
	ω-3 fatty acid	Fatty acid re-esterification and enhanced FAO	Improved diabetes and hepatic steatosis	(136)
	NADPH oxidase inhibitor	Reduces ROS and prevents OXPHOS dysfunction	Improved glucose and insulin tolerance	(137)
	Notch inhibitor (DAPT)	Impairs glucose oxidation and ROS generation	Notch1 deficiency mitigates steatohepatitis	(138)
	mTOR inhibitor	Torin but not rapamycin suppresses glucose uptake	Resveratrol prevents glucose tolerance	(71, 139)
Atherosclerosis	IL-13	Increases mitochondrial biogenesis and activity	Reduced macrophagesin atherosclerotic plaques	(116)
	LXR agonist (desmosterol)	Alters fatty acid and cholesterol metabolism	Deactivated foam cells with reduced inflammation	(140)
	PKM2 inhibitor	PKM2 deficiency reduces glycolysis	Mitigated atherosclerotic lesion formation	(141)
	AMPK activator (anti-miR-33)	Increases OXPHOS and reduces glycolysis	Regressed atherosclerotic plaques	(133)
	Autophagy	Suppresses glucose consumption	ATG5 deficiency enhanced atherosclerotic plaque formation	(142)