J Clin Invest. 2020 Aug 3;130(8):3968-3970. doi: 10.1172/JCI138536.
Atherosclerosis is an inflammatory condition of the arteries that has profound incidence and increasing prevalence. Although endothelial cells detect changes in blood flow, how endothelial activation contributes to atherogenic inflammation is not well understood. In this issue of the JCI, Alfaidi et al. used mouse models to explore flow-induced endothelial activation. The authors revealed a role for Nck1 and a specific activator of the innate immune response, the downstream interleukin receptor-associated kinase-1 (IRAK-1) in NF-κB-mediated inflammation and atherosclerosis susceptibility. These results link disturbed blood flow to NF-κB-mediated inflammation, which promotes atherosclerosis, and provide Nck1 as a potential target for the treatment of atherosclerosis.
动脉粥样硬化是一种影响深远且日益普遍的动脉炎症疾病。尽管内皮细胞可以检测到血流的变化，但内皮细胞的激活如何导致动脉粥样硬化炎症尚不清楚。在本期 JCI 中，Alfaidi 等人利用小鼠模型探索了血流诱导的内皮细胞激活。作者揭示了 Nck1 和先天免疫反应的特定激活物下游白细胞介素受体相关激酶-1（IRAK-1）在 NF-κB 介导的炎症和动脉粥样硬化易感性中的作用。这些结果将血流紊乱与促进动脉粥样硬化的 NF-κB 介导的炎症联系起来，并为 Nck1 作为动脉粥样硬化治疗的潜在靶点提供了依据。
