2024-03-28T21:00:52Zhttp://repisalud.isciii.es/oai/requestoai:repisalud.isciii.es:20.500.12105/76632022-11-08T11:42:01Zcom_20.500.12105_2145com_20.500.12105_2051com_20.500.12105_2144col_20.500.12105_2146
Repisalud
author
Andres, Vicente
author
Pello, Oscar M
author
Silvestre-Roig, Carlos
funder
Ministerio de Economía y Competitividad (España)
funder
Instituto de Salud Carlos III
funder
Unión Europea. Comisión Europea
funder
Belgian Society of Cardiology
funder
Fundación Mario Losantos del Campo
funder
Fundación Ferrer Investigación
funder
Fundación ProCNIC
2019-05-23T09:51:20Z
2019-05-23T09:51:20Z
2012-10
Curr Opin Lipidol. 2012; 23(5):429-38
0957-9672
http://hdl.handle.net/20.500.12105/7663
22964992
10.1097/MOL.0b013e328357a379
1473-6535
Current opinion in lipidology
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.
eng
Macrophage proliferation and apoptosis in atherosclerosis
journal article
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URL
https://repisalud.isciii.es/bitstream/20.500.12105/7663/1/MacrophageProliferationApoptosisAtherosclerosis_2012.pdf
File
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application/pdf
MacrophageProliferationApoptosisAtherosclerosis_2012.pdf
URL
https://repisalud.isciii.es/bitstream/20.500.12105/7663/3/MacrophageProliferationApoptosisAtherosclerosis_2012.pdf.txt
File
MD5
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text/plain
MacrophageProliferationApoptosisAtherosclerosis_2012.pdf.txt