Macrophage Trafficking, Inflammatory Resolution, and Genomics in Atherosclerosis: JACC Macrophage in CVD Series (Part 2).

Macrophage Trafficking, Inflammatory Resolution, and Genomics in Atherosclerosis: JACC Macrophage in CVD Series (Part 2).
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DOI:
10.1016/j.jacc.2018.08.2147
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发表时间:
2018-10-30
影响因子:
24
通讯作者:
Kovacic JC
Kovacic JC
中科院分区:
医学1区
文献类型:
--
作者:
Moore KJ;Koplev S;Fisher EA;Tabas I;Björkegren JLM;Doran AC;Kovacic JC

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Atherosclerosis is characterized by the retention of modified lipoproteins in the arterial wall. These modified lipoproteins activate resident macrophages, and the recruitment of monocyte-derived cells, which differentiate into mononuclear phagocytes that ingest the deposited lipoproteins to become “foam cells”; a hallmark of this disease. In this part 2 of a 4-part review series covering the macrophage in cardiovascular disease, we critically review the contributions and relevant pathobiology of monocytes, macrophages and foam cells as relevant to atherosclerosis. We also review evidence that via various pathways, a failure of the resolution of inflammation is an additional key aspect of this disease process. Finally, we consider the likely role played by genomics and biologic networks in controlling the macrophage phenotype in atherosclerosis. Collectively, these data provide substantial insights on the atherosclerotic process, while concurrently offering numerous molecular and genomic candidates that appear to hold great promise for selective targeting as clinical therapies. Atherosclerosis is characterized by the retention of modified lipoproteins in the arterial wall. These modified lipoproteins activate resident macrophages, and the recruitment of monocyte-derived cells, which differentiate into mononuclear phagocytes that ingest the deposited lipoproteins to become “foam cells”; a hallmark of this disease. In this second of a 4-part review series we consider the contributions and pathobiology of monocytes, macrophages and foam cells as relevant to atherosclerosis. We also review evidence that failure of inflammation resolution is a key aspect of this disease, and also the role of genomics and biologic networks in controlling the macrophage phenotype in atherosclerosis.
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