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Myeloid-Specific IκB Kinase β Deficiency Decreases Atherosclerosis in Low-Density Lipoprotein Receptor–Deficient Mice
Author(s) -
Sehyung Park,
Yipeng Sui,
Florence Gizard,
Jinxian Xu,
Jennifer Rios-Pilier,
Robert N. Helsley,
SeongSu Han,
Changcheng Zhou
Publication year - 2012
Publication title -
arteriosclerosis thrombosis and vascular biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.007
H-Index - 270
eISSN - 1524-4636
pISSN - 1079-5642
DOI - 10.1161/atvbaha.112.254573
Subject(s) - iκb kinase , inflammation , macrophage , foam cell , myeloid , lipoprotein , immunology , proinflammatory cytokine , medicine , ldl receptor , cancer research , biology , nf κb , cholesterol , biochemistry , in vitro
Inflammatory responses are the driving force of atherosclerosis development. IκB kinase β (IKKβ), a central coordinator in inflammation through regulation of nuclear factor-κB, has been implicated in the pathogenesis of atherosclerosis. Macrophages play an essential role in the initiation and progression of atherosclerosis, yet the role of macrophage IKKβ in atherosclerosis remains elusive and controversial. This study aims to investigate the impact of IKKβ expression on macrophage functions and to assess the effect of myeloid-specific IKKβ deletion on atherosclerosis development.

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