Author(s): Lundberg AM, Yan ZQ
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Abstract PURPOSE OF REVIEW: 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. RECENT FINDINGS: 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. SUMMARY: 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.
This article was published in Curr Opin Lipidol
and referenced in Internal Medicine: Open Access