Macrophages play central roles in the initiation, growth, and ultimately rupture of atherosclerotic plaques. Altered metabolism is the key feature that dictates macrophage function and subsequent disease progression. This review explores how the core factors of plaque microenvironment shape the metabolic rewiring of macrophages in atherosclerosis as well as how these metabolic shifts in turn alter the immune-effector and tissue-reparative functions of macrophage. Finally, this review offers insight into the challenges and opportunities of using immune metabolism to modulate macrophage responses in disease.