Karolinska Institute, Center for Molecular Medicine, L8:03, Karolinska University Hospital, SE-17176 Stockholm, Sweden.
Curr Opin Lipidol. 2011 Oct;22(5):343-9. doi: 10.1097/MOL.0b013e32834ada80.
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.
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.
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.
强调过去一年中在研究内源性促动脉粥样硬化危险信号以及动脉粥样硬化中固有免疫信号转导的相应分子机制方面取得的重要进展。
了解修饰 LDL 在动脉粥样硬化发展中的致病作用的核心在于 LDL 衍生的炎症成分的特性和信号转导机制。前几年的研究揭示了 LDL 衍生的磷脂和胆固醇晶体作为内源性危险信号。这些危险信号分别触发 Toll 样受体和核苷酸结合寡聚结构域样受体炎性小体，从而引发炎症反应并促进疾病进展。
最近对 LDL 在动脉粥样硬化中的因果作用的理解为修饰 LDL 衍生的危险信号提供了一个新的视角。这些发现提示，Toll 样受体和核苷酸结合寡聚结构域炎性小体信号失调是动脉粥样形成的重要机制。
