Suppr超能文献

炎性小体与动脉粥样硬化形成

Inflammasome and atherogenesis.

作者信息

Lu Xinjie, Kakkar Vijay

机构信息

Thrombosis Research Institute, London, SW3 6LR.

出版信息

Curr Pharm Des. 2014;20(1):108-24. doi: 10.2174/13816128113199990586.

Abstract

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.

摘要

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。

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验