Macrophage death and defective inflammation resolution in atherosclerosis.
A key event in atherosclerosis is a maladaptive inflammatory response to subendothelial lipoproteins. A crucial aspect of this response is a failure to resolve inflammation, which normally involves the suppression of inflammatory cell influx, effective clearance of apoptotic cells and promotion of inflammatory cell egress. Defects in these processes promote the progression of atherosclerotic lesions into dangerous plaques, which can trigger atherothrombotic vascular disease, the leading cause of death in industrialized societies. In this Review I provide an overview of these concepts, with a focus on macrophage death and defective apoptotic cell clearance, and discuss new therapeutic strategies designed to boost inflammation resolution in atherosclerosis.
Tabas
Ira
I
Department of Medicine, Physiology and Cellular Biophysics, Columbia University, New York, New York 10032, USA. iat1@columbia.edu
D000818:Animals; D017209:Apoptosis / Q000276:immunology*; D050197:Atherosclerosis / Q000276:immunology / Q000473:pathology* / Q000628:therapy; D006801:Humans; D007249:Inflammation / Q000276:immunology / Q000473:pathology / Q000628:therapy; D008262:Macrophage Activation / Q000276:immunology; D008264:Macrophages / Q000276:immunology / Q000473:pathology*; D010587:Phagocytosis / Q000276:immunology