title: Toll-like receptors in atherosclerosis.
abstract: Atherosclerosis, the leading cause of cardiovascular disease (CVD), is driven by inflammation. Increasing evidence suggests that toll-like receptors (TLRs) are key orchestrators of the atherosclerotic disease process. Interestingly, a distinct picture is being revealed for individual receptors in atherosclerosis. TLRs exhibit a complex nature enabling the detection of multiple motifs named danger-associated molecular patterns (DAMPs) and pathogen-associated molecular patterns (PAMPs). Activation of these receptors triggers an intracellular signalling cascade mediated through MyD88 or TRIF, leading to the production of pro- and anti-inflammatory cytokines. In this review we explore key novel findings pertaining to TLR signalling in atherosclerosis, including recently described endosomal TLRs and future directions in TLR research.
authors.affiliation: Kennedy Institute of Rheumatology, NDORMS, University of Oxford, Roosevelt Drive, Headington, Oxford OX3 7FY, UK. m.falck-hansen09@imperial.ac.uk
authors.forename: Mika
authors.initials: M
authors.lastname: Falck-Hansen
authors.forename: Christina
authors.initials: C
authors.lastname: Kassiteridi
authors.forename: Claudia
authors.initials: C
authors.lastname: Monaco
mesh_terms: D000818:Animals; D001057:Apolipoproteins E / Q000235:genetics / Q000378:metabolism; D050197:Atherosclerosis / Q000378:metabolism* / Q000473:pathology; D006801:Humans; D053594:Myeloid Differentiation Factor 88 / Q000378:metabolism; D012307:Risk Factors; D015398:Signal Transduction; D051193:Toll-Like Receptors / Q000378:metabolism*
chemical_list: D001057:Apolipoproteins E; D053594:Myeloid Differentiation Factor 88; D051193:Toll-Like Receptors