Self-eating in the plaque: what macrophage autophagy reveals about atherosclerosis

• Autophagy is a critical degradation process in macrophages.
• Recent data link defects in macrophage autophagy to the progression of atherosclerosis.
• Macrophage autophagy has roles in cholesterol homeostasis, oxidative stress, and inflammatory signaling.
• Harnessing the autophagic response in macrophages holds immense therapeutic potential.

Autophagy (or ‘self-eating’) is the process by which cellular contents are recycled to support downstream metabolism. An explosion in research in the past decade has implicated its role in both health and disease and established the importance of the autophagic response during periods of stress and nutrient deprivation. Atherosclerosis is a state where chronic exposure to cellular stressors promotes disease progression, and alterations in autophagy are predicted to be consequential. Recent reports linking macrophage autophagy to lipid metabolism, blunted inflammatory signaling, and an overall suppression of proatherogenic processes support this notion. We review these data and provide a framework for understanding the role of macrophage autophagy in the pathogenesis of atherosclerosis, one of the most formidable diseases of our time.