From the Department of Cardiology and Angiology I, University Heart Center Freiburg, Germany (D.W.).
Faculty of Medicine, University of Freiburg, Germany (D.W.).
Circ Res. 2019 Jan 18;124(2):315-327. doi: 10.1161/CIRCRESAHA.118.313591.
There is now overwhelming experimental and clinical evidence that atherosclerosis is a chronic inflammatory disease. Lessons from genome-wide association studies, advanced in vivo imaging techniques, transgenic lineage tracing mice, and clinical interventional studies have shown that both innate and adaptive immune mechanisms can accelerate or curb atherosclerosis. Here, we summarize and discuss the pathogenesis of atherosclerosis with a focus on adaptive immunity. We discuss some limitations of animal models and the need for models that are tailored to better translate to human atherosclerosis and ultimately progress in prevention and treatment.
现在有压倒性的实验和临床证据表明,动脉粥样硬化是一种慢性炎症性疾病。全基因组关联研究、先进的体内成像技术、转基因谱系追踪小鼠和临床干预研究的结果表明,固有免疫和适应性免疫机制都可以加速或抑制动脉粥样硬化的发生。在这里,我们总结并讨论了动脉粥样硬化的发病机制,重点是适应性免疫。我们讨论了一些动物模型的局限性,以及需要定制更适合人类动脉粥样硬化的模型,以最终促进预防和治疗的进展。