title: Novel immune signals and atherosclerosis.
abstract: Atherosclerosis underlies coronary artery disease (CAD) and cerebrovascular disease, which are the most common forms of life-threatening cardiovascular disorders. To minimize the risk of atherosclerotic complications, primary and secondary prevention strategies seek to control risk factors. Reducing low-density lipoprotein (LDL) cholesterol through lipid-lowering drugs, such as statins, in particular yields a proportional decrease in cardiovascular disease risk. Atherosclerosis is considered to be a complex chronic inflammatory process triggered by cardiovascular risk factors which cause endothelial dysfunction and inflammatory cell infiltration within the artery wall. In this review, we summarize the current understanding of the underling molecular mechanisms of the immune signals in the development and progression of atherosclerosis. Among various molecular mechanisms, toll like receptors (TLRs) are potent proinflammatory cytokines that operate to induce inflammation play an important role in the pathogenesis of atherosclerosis. Moreover, we discuss current knowledge regarding monocyte/macrophage biology that contributes to the progression of atherosclerosis, including macrophage polarization and heterogeneity. Understanding the molecular mechanisms in conjunction with orchestration of monocyte/macrophage biology should provide a basis for novel treatment strategies to prevent the development and progression of atherosclerosis.
authors.affiliation: Brigham and Women's Hospital, Department of Medicine, Cardiovascular Division, Center for Interdisciplinary Cardiovascular Sciences, 3 Blackfan Street, 17th Floor, Boston, MA 02115, USA. hiroiwata-circ@umin.ac.jp
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Iwata
authors.forename: Ryozo
authors.initials: R
authors.lastname: Nagai
mesh_terms: D000818:Animals; D050197:Atherosclerosis / Q000276:immunology* / Q000473:pathology / Q000503:physiopathology; D003324:Coronary Artery Disease / Q000503:physiopathology; D006801:Humans; D008264:Macrophages / Q000276:immunology; D009000:Monocytes / Q000276:immunology; D012307:Risk Factors; D015398:Signal Transduction