Department of General Biochemistry, Faculty of Biology and Environmental Protection, University of Lodz, Pomorska 141/143, 90-236 Lodz, Poland.
Biohazard Prevention Centre, Faculty of Biology and Environmental Protection, University of Lodz, Pomorska 141/143, 90-236 Lodz, Poland.
Int J Mol Sci. 2022 Apr 30;23(9):5017. doi: 10.3390/ijms23095017.
The pathophysiology of atherosclerosis and acute coronary syndrome (ACS) is related to interactions between immune cells, endothelium, and blood platelets. An increasing number of reports confirm the link between excessive immune activation and cellular cross-talk with ACS incidence. Our genetic and proteomic analysis was performed on strictly selected atherosclerotic patients with non-fatal ACS without typical risk factors and healthy donors. Results showed changes in the gene expression levels of the various inflammatory factors derived from the peripheral blood cells that drive the over-activation of the immune system. The enhanced activation of the immune system may lead to the overexpression of the pro-inflammatory mediators, which causes self-perpetuating machinery of processes associated with thrombosis. In our preliminary study, we confirmed an altered expression of genes associated with the inflammation and overall interaction of the vascular microenvironment. Furthermore, 5 of 92 analyzed genes, , , , , and , were expressed only in patients with ACS. In conclusion, the augmented expression of the pro-inflammatory genes from the peripheral blood cells may be a crucial genetic factor leading to the occurrence of acute inflammation and thus be significant in ACS pathogenesis.
动脉粥样硬化和急性冠状动脉综合征 (ACS) 的病理生理学与免疫细胞、内皮细胞和血小板之间的相互作用有关。越来越多的报告证实,过度的免疫激活与 ACS 发生率之间存在细胞串扰之间存在关联。我们对没有典型风险因素的非致命性 ACS 且严格选择的动脉粥样硬化患者和健康供体进行了遗传和蛋白质组学分析。结果显示,源自外周血细胞的各种炎症因子的基因表达水平发生了变化,这些因子驱动免疫系统过度激活。免疫系统的过度激活可能导致促炎介质的过度表达,从而导致与血栓形成相关的自我维持过程。在我们的初步研究中,我们证实了与炎症和血管微环境整体相互作用相关的基因表达发生了改变。此外,在分析的 92 个基因中,有 5 个仅在 ACS 患者中表达,分别是、、、和。总之,外周血细胞中促炎基因的表达增加可能是导致急性炎症发生的关键遗传因素,因此在 ACS 发病机制中具有重要意义。