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Trends Endocrinol Metab. 2014 May;25(5):225-34. doi: 10.1016/j.tem.2014.03.010. Epub 2014 Apr 17.

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

Author information

1
Cardiovascular Division, Department of Medicine, Washington University School of Medicine, St Louis, MO 63110, USA.
2
Cardiovascular Division, Department of Medicine, Washington University School of Medicine, St Louis, MO 63110, USA; Department of Pathology and Immunology, Washington University School of Medicine, St Louis, MO 63110, USA. Electronic address: brazani@im.wustl.edu.

Abstract

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.

KEYWORDS:

atherosclerosis; autophagy; inflammation; lipid metabolism; macrophage

PMID:
24746519
PMCID:
PMC4061377
DOI:
10.1016/j.tem.2014.03.010
[Indexed for MEDLINE]
Free PMC Article

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