Journal
CURRENT OPINION IN LIPIDOLOGY
Volume 23, Issue 5, Pages 429-438Publisher
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1097/MOL.0b013e328357a379
Keywords
apoptosis; atherosclerosis; cell proliferation; macrophage
Funding
- Ministerio de Economia y Competitividad (MINECO) [SAF2010-16044]
- Instituto de Salud Carlos III [RD06/0014/0021 (RECAVA)]
- European Commission [PCIG10-GA-2011-303850]
- Belgian Society of Cardiology
- Fundacion Mario Losantos del Campo
- Fundacion Ferrer para la Investigacion
- MINECO
- Pro-CNIC Foundation
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Purpose of review Atherosclerosis is driven by cardiovascular risk factors that cause the recruitment of circulating immune cells beneath the vascular endothelium. Infiltrated monocytes differentiate into different macrophage subtypes with protective or pathogenic activities in vascular lesions. We discuss current knowledge about the molecular mechanisms that regulate lesional macrophage proliferation and apoptosis, two processes that occur during atherosclerosis development and regulate the number and function of macrophages within the atherosclerotic plaque. Recent findings Lesional macrophages in early phases of atherosclerosis limit disease progression by phagocytizing modified lipoproteins, cellular debris and dead cells that accumulate in the plaque. However, macrophages in advanced lesions contribute to a maladaptive, nonresolving inflammatory response that can lead to life-threatening acute thrombotic diseases (myocardial infarction or stroke). Macrophage-specific manipulation of genes involved in cell proliferation and apoptosis modulates lesional macrophage accumulation and atherosclerosis burden in mouse models, and studies are beginning to elucidate the underlying mechanisms. Summary Despite recent advances in our understanding of macrophage proliferation and apoptosis in atherosclerotic plaques, it remains unclear whether manipulating these processes will be beneficial or harmful. Advances in these areas may translate into more efficient therapies for the prevention and treatment of atherothrombosis.
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