Abstract：
Atherosclerosis (AS) is a chronic inflammatory vascular disease that begins with endothelial activation followed by a series of inflammatory responses, plaque formation, and finally rupture. An early event in endothelial dysfunction is activation of the nuclear factor-κB (NF-κB) signaling axis. Toll-like receptors (TLRs) in endothelial cells (ECs) play an essential role in recognizing pathogen-associated molecular patterns (PAMPs), damage-associated molecular patterns (DAMPs), and lifestyle-associated molecular patterns (LAMPs). Activation of the canonical NF-κB pathway stimulates the expression of cytokines, chemokines, and an array of additional genes which activate and amplify AS-associated inflammatory responses. In this review, we discuss the involvement of TLR2/4 and NF-κB signaling in ECs during AS initiation, as well as regulation of the inflammatory response during AS by noncoding RNAs, especially microRNA (miRNA) and circular RNA (circRNA).
摘要：
动脉粥样硬化（AS）是一种慢性炎症性血管疾病，始于内皮激活，然后是一系列炎症反应，斑块形成,最后破裂。内皮功能障碍的早期事件是核因子-κB（NF-κB）信号轴的激活。内皮细胞中的Toll样受体（TLRs）在识别病原体相关分子模式（PAMPs）中起着至关重要的作用。损伤相关分子模式(DAMPs)，和生活方式相关的分子模式(LAMMPs)。经典NF-κB途径的激活刺激细胞因子的表达，趋化因子,以及一系列激活和放大AS相关炎症反应的额外基因。在这次审查中,我们讨论了TLR2/4和NF-κB信号在AS开始时参与ECs，以及通过非编码RNA调节AS期间的炎症反应，特别是microRNA(miRNA)和环状RNA(circularRNA)。
