期刊
CIRCULATION RESEARCH
卷 119, 期 3, 页码 414-417出版社
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1161/CIRCRESAHA.116.309194
关键词
atherosclerosis; bone marrow; macrophage; myocardial; infarction; monocyte
资金
- National Institutes of Health (NIH) [HL096576, HL095629, NS084863, HL128264, HL095612]
The heart and blood vessels of a healthy individual contain resident immune cells, the majority of which are macrophages that have seeded these organs early in the development. In the mouse, approximate to 10% of noncardiomyocytes are macrophages, 1,2 and humans may have comparable numbers. 1 After myocardial infarction, macrophage numbers increase in the heart through the combined effects of massive recruitment of bone marrow-derived cells and local self-renewal. 1,3 Likewise, in atherosclerosis, the chronic lipid-driven inflammatory disease that is the underlying cause of myocardial infarction, macrophage numbers increase in the vessel wall, again because of recruitment and local proliferation. 4 Although many of these insights have been generated in mouse models, compelling evidence from genome-wide association studies have associated innate immunity mediators with myocardial infarction, 5 whereas prospective human studies have shown that blood monocyte levels can predict cardiovascular events in patients. 6
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