巨噬细胞
细胞代谢
效应器
细胞生物学
生物
免疫系统
免疫学
巨噬细胞极化
新陈代谢
内分泌学
生物化学
体外
作者
Graeme J. Koelwyn,Emma M. Corr,Ebru Erbay,Kathryn J. Moore
标识
DOI:10.1038/s41590-018-0113-3
摘要
After activation, cells of the myeloid lineage undergo robust metabolic transitions, as well as discrete epigenetic changes, that can dictate both ongoing and future inflammatory responses. In atherosclerosis, in which macrophages play central roles in the initiation, growth, and ultimately rupture of arterial plaques, altered metabolism is a key feature that dictates macrophage function and subsequent disease progression. This Review explores how factors central to the plaque microenvironment (for example, altered cholesterol metabolism, oxidative stress, hypoxia, apoptotic and necrotic cells, and hyperglycemia) shape the metabolic rewiring of macrophages in atherosclerosis as well as how these metabolic shifts in turn alter macrophage immune-effector and tissue-reparative functions. Finally, this overview offers insight into the challenges and opportunities of harnessing metabolism to modulate aberrant macrophage responses in disease. In this Review, Moore and colleagues discuss regulation of macrophage immunometabolism in atherosclerosis.
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