Miteva Kapka, Madonna Rosalinda, De Caterina Raffaele, Van Linthout Sophie
Department of Biomedical Sciences, Adaptive Immunity Laboratory, Humanitas Clinical and Research Center, Rozzano, Milano, Italy.
Center of Aging Sciences and Translational Medicine - CESI-MeT, Institute of Cardiology, Department of Neurosciences, Imaging and Clinical Sciences, "G. d'Annunzio" University, Chieti, Italy.
Vascul Pharmacol. 2018 Apr 22. doi: 10.1016/j.vph.2018.04.006.
Atherosclerosis is a chronic inflammatory disorder of the large and medium-size arteries characterized by the subendothelial accumulation of cholesterol, immune cells, and extracellular matrix. At the early onset of atherogenesis, endothelial dysfunction takes place. Atherogenesis is further triggered by the accumulation of cholesterol-carrying low-density lipoproteins, which acquire properties of damage-associated molecular patterns and thereby trigger an inflammatory response. Following activation of the innate immune response, mainly governed by monocytes and macrophages, the adaptive immune response is started which further promotes atherosclerotic plaque formation. In this review, an overview is given describing the role of damage-associated molecular patterns, NLRP3 inflammasome activation, and innate and adaptive immune cells in the atherogenesis process.
动脉粥样硬化是一种发生在大中型动脉的慢性炎症性疾病，其特征是胆固醇、免疫细胞和细胞外基质在内皮下堆积。在动脉粥样硬化形成的早期，会发生内皮功能障碍。携带胆固醇的低密度脂蛋白的堆积进一步触发了动脉粥样硬化的形成，这些低密度脂蛋白获得了损伤相关分子模式的特性，从而引发炎症反应。在主要由单核细胞和巨噬细胞主导的固有免疫反应激活后，启动适应性免疫反应，这进一步促进动脉粥样硬化斑块的形成。在这篇综述中，概述了损伤相关分子模式、NLRP3炎性小体激活以及固有免疫细胞和适应性免疫细胞在动脉粥样硬化形成过程中的作用。
