title: Innate immune recognition receptors and damage-associated molecular patterns in plaque inflammation.
abstract: OBJECTIVE
  To highlight critical advances achieved over the last year in the study of endogenous proatherogenic danger signals and corresponding molecular mechanism of innate immune signalling in atherosclerosis.
  
  
  RESULTS
  The identity and signalling mechanisms of LDL-derived inflammatory components are central in understanding the pathogenic role of modified LDL in the development of atherosclerosis. Studies in the preceding years have revealed LDL-derived phospholipids and cholesterol crystals as endogenous danger signals. These danger signals trigger Toll-like receptors and nucleotide-binding oligomerization domain-like receptors inflammasome respectively, thereby instigating inflammatory responses and promoting disease progression.
  
  
  CONCLUSIONS
  Recent understandings of the causal role of LDL in atherosclerosis provide a new perspective on modified LDL-derived danger signals. These insights suggest dysregulated Toll-like receptor and nucleotide-binding oligomerization domain inflammasome signalling as an important mechanism underlying atherogenesis.
authors: Karolinska Institute, Center for Molecular Medicine, L8:03, Karolinska University Hospital, SE-17176 Stockholm, Sweden.
authors: Anna M
authors: AM
authors: Lundberg
authors: Zhong-qun
authors: ZQ
authors: Yan
mesh_terms: D000818:Animals; D050197:Atherosclerosis / Q000276:immunology*; D006801:Humans; D007113:Immunity, Innate / Q000276:immunology*; D007249:Inflammation / Q000276:immunology*; D008077:Lipoproteins, LDL / Q000378:metabolism; D051193:Toll-Like Receptors / Q000378:metabolism
chemical_list: D008077:Lipoproteins, LDL; D051193:Toll-Like Receptors