Lu Xinjie, Kakkar Vijay
Thrombosis Research Institute, London, SW3 6LR.
Curr Pharm Des. 2014;20(1):108-24. doi: 10.2174/13816128113199990586.
Atherosclerosis is a progressive disease starting with accumulation of lipids, lipoproteins, and immune cells in the arterial wall. Inflammation and the innate immune response are involved in the formation of early atherosclerotic lesion. A protein complex known as the inflammasome is stimulated to activate interleukin-1β (IL-1β) and IL-18, which are responsible for activation of inflammatory processes. Inflammasome-mediated processes are important in the process of atherosclerosis. The front of structure domains as well as IL-1, and IL-18 stands at the threshold of the adaptive immune response that accelerates full-blown atherosclerotic disease progression. This review is intended to provide new insights into the pathogenesis of atherosclerosis and indicate new potential molecular targets for therapy of this disease.
动脉粥样硬化是一种渐进性疾病，始于脂质、脂蛋白和免疫细胞在动脉壁的积聚。炎症和先天免疫反应参与早期动脉粥样硬化病变的形成。一种称为炎性小体的蛋白质复合物被刺激激活白细胞介素-1β（IL-1β）和IL-18，它们负责激活炎症过程。炎性小体介导的过程在动脉粥样硬化过程中很重要。结构域前沿以及IL-1和IL-18处于适应性免疫反应的阈值，该反应加速了全面动脉粥样硬化疾病的进展。本综述旨在为动脉粥样硬化的发病机制提供新见解，并指出该疾病治疗的新潜在分子靶点。
