Gwendalyn J Randolph1. 1. Department of Gene and Cell Medicine, and the Immunology Institute, 1425 Madison Avenue, Mount Sinai School of Medicine, New York 10029, USA. gwendalyn.randolph@mssm.edu
Abstract
PURPOSE OF REVIEW: This review compares the fate of monocyte-derived cells that enter atherosclerotic plaques with those that accumulate at other sites of inflammation. RECENT FINDINGS: Resolution of inflammatory reactions involves emigration of monocyte-derived cells out of the inflamed site through nearby lymphatic vessels. However, this emigratory process associated with resolution is impaired in atherosclerosis. The mechanism for impeded emigration from plaques in vivo remains to be determined, but multiple factors are likely involved, including specialized properties of artery walls and a negative impact of lipid mediators on monocyte-derived cell migration. SUMMARY: Impaired egress would be expected to compound macrophage accumulation within plaques, contribute to build-up of necrotic pools, and explain in part the reticence of many plaques to regress, or resolve. Restoration of the capacity of monocyte-derived cells to leave plaques would, by contrast, be expected to facilitate regression, but it remains to be determined whether restoring egress may sometimes provoke unwanted outcomes as well.
PURPOSE OF REVIEW: This review compares the fate of monocyte-derived cells that enter atherosclerotic plaques with those that accumulate at other sites of inflammation. RECENT FINDINGS: Resolution of inflammatory reactions involves emigration of monocyte-derived cells out of the inflamed site through nearby lymphatic vessels. However, this emigratory process associated with resolution is impaired in atherosclerosis. The mechanism for impeded emigration from plaques in vivo remains to be determined, but multiple factors are likely involved, including specialized properties of artery walls and a negative impact of lipid mediators on monocyte-derived cell migration. SUMMARY: Impaired egress would be expected to compound macrophage accumulation within plaques, contribute to build-up of necrotic pools, and explain in part the reticence of many plaques to regress, or resolve. Restoration of the capacity of monocyte-derived cells to leave plaques would, by contrast, be expected to facilitate regression, but it remains to be determined whether restoring egress may sometimes provoke unwanted outcomes as well.
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