NLRP3炎性小体、胆固醇结晶与动脉粥样硬化关系的研究进展

Roles of NLRP3 inflammasome and cholesterol crystals in the development of atherosclerosis

动脉粥样硬化(AS)与血管内皮功能障碍、炎症、自身免疫等多种因素有关,是以血管壁炎症反应为基础的慢性病理过程。近来研究表明,炎性小体(Inflammasome)是炎症反应的核心。炎性小体作为固有免疫的一种模式识别受体,通过激活半胱氨酸天冬氨酸特异性蛋白酶1(Caspase1),介导炎性因子的分泌,参与各种炎症性疾病包括动脉粥样硬化的发生发展。胆固醇结晶被认为是动脉粥样硬化病变的标志,作为内源性物质之一能激活NOD样受体蛋白3(NLRP3)炎性小体,促进动脉粥样硬化的发展。为了给研究动脉粥样硬化抗炎症治疗提供新思路、新靶点,我们现将炎性小体活化及调控与胆固醇结晶、动脉粥样硬化关系研究进展做一综述。

Atherosclerosis(AS) is the chronic inflammation of the blood vessel wall, which is associated with a variety of factors such as vascular endothelial dysfunction, inflammation and autoimmune. Recent studies have shown that the inflammasome is the core of the inflammatory response. Inflammasome, one of the innate immune pattern recognition receptors, can activate Cysteine aspartate-specific protease 1(Caspase 1) and promote the release of inflammatory cytokines, then participate in the development of many inflammatory diseases including atherosclerosis. Cholesterol crystals are the sign of atherosclerotic lesions. As one of endogenous substances, they can activate the NOD-like receptor protein 3(NLRP3) inflammasome and promote the development of atherosclerosis. For providing a new target for anti-inflammatory therapy, this article will focus on the roles of inflammasome and cholesterol crystals in the development of atherosclerosis.