Atherosclerosis is an arterial disease associated with dyslipidemia, abnormal arterial calcification and oxidative stress. It has been shown that a continued chronic inflammatory state of the arterial wall contributes to the development of atherosclerosis. The inflammatory stimulation, recruitment of inflammatory cells and production of pro-inflammatory cytokines enhances vascular inflammation. Some members of the S100 proteins family bind with their receptors, such as advanced glycation end products (RAGE), scavenger receptors (CD36) and toll-like receptor 4 (TLR-4), contributing to the cellular response in atherosclerotic progression. This review summarizes the roles of S100 proteins (S100A8, S100A9 and S100A12) in the vascular inflammation, vascular calcification and vascular oxidative stress. S100 proteins are released from monocytes, smooth muscle cells and endothelial cells in response to cellular stress stimuli, and then the binding of S100 proteins to RAGE activate downstream signaling such as transcription factor kappa B (NF-κB) translocation and reactive oxygen species (ROS) production, which act as a positive feedback loop for inducing pro-inflammatory phenotype in a wide variety of cell types including endothelial cells, vascular smooth muscle cells and leukocytes. Thus, it suggests that the inhibition of S100 proteins-mediated RAGE and TLR4 activation appears to be a promising approach to treat atherosclerosis. In addition, recent study showed that serum S100A12 can predict future cardiovascular events, highlighting that S100A12 is likely to be a potential biomarker of therapeutic efficacy and disease progression in coronary heart disease. Future studies of patients with coronary heart disease may provide more evidences supporting that S100 proteins is promising drug target in the prevention and therapy of atherosclerosis.

中文翻译：

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S100蛋白在动脉粥样硬化中。

动脉粥样硬化是与血脂异常，动脉钙化异常和氧化应激相关的动脉疾病。已经显示，动脉壁的持续慢性炎症状态有助于动脉粥样硬化的发展。炎症刺激，炎症细胞募集和促炎细胞因子的产生增强了血管炎症。S100蛋白家族的某些成员与其受体结合，例如晚期糖基化终产物（RAGE），清除剂受体（CD36）和Toll样受体4（TLR-4），有助于动脉粥样硬化进程中的细胞反应。这篇综述总结了S100蛋白（S100A8，S100A9和S100A12）在血管炎症，血管钙化和血管氧化应激中的作用。S100蛋白从单核细胞释放，平滑肌细胞和内皮细胞响应细胞应激刺激，然后S100蛋白与RAGE的结合激活下游信号传导，例如转录因子kappa B（NF-κB）易位和活性氧（ROS）的产生，正反馈回路，可在多种细胞类型（包括内皮细胞，血管平滑肌细胞和白细胞）中诱导促炎表型。因此，这表明抑制S100蛋白介导的RAGE和TLR4活化似乎是治疗动脉粥样硬化的有前途的方法。此外，最近的研究表明，血清S100A12可以预测未来的心血管事件，突显了S100A12可能是冠心病的治疗功效和疾病进展的潜在生物标志物。