HCC-1（hemofiltrate CC chemokine-1）是一种 CC 型趋化因子，发挥改变细胞内钙浓度、诱导白细胞和操纵酶释放的功能，尤其是在单核细胞中。据报道，HCC-1可以通过调节细胞周期和促进细胞凋亡来预测持续性急性肾损伤或抑制肝细胞癌，但HCC-1对动脉粥样硬化的作用尚不清楚。本研究旨在阐明HCC-1在动脉粥样硬化中的功能和机制，以及其是否可以作为诊断动脉粥样硬化的新型生物标志物。HCC-1在动脉粥样硬化患者血清、动脉粥样硬化斑块和正常动脉组织中的表达情况对照组通过ELISA、免疫组织化学和共聚焦显微镜以及生物信息分析进行评估。 HCC-1 过表达小鼠和对照小鼠的动脉粥样硬化模型是通过在 ApoE-/- 背景下尾静脉注射腺相关病毒血清型 9-HCC-1 产生的。在体外评估细胞粘附、极化和细胞焦亡。分析动脉粥样硬化患者血清中 HCC-1 浓度与动脉粥样硬化的关系。生物信息学分析显示，HCC-1 表达与动脉粥样硬化的发生及稳定-不稳定转换呈正相关，HCC-1 升高的结果进一步支持了这一点。 AS 患者血清和动脉粥样硬化斑块中均表达 1。腺相关病毒血清型9-HCC-1小鼠炎症因子水平较高，斑块中巨噬细胞积累和焦亡率增加，动脉粥样硬化斑块稳定性降低。在体外，HCC-1 促进单核细胞粘附和 M1 极化，并诱导 EC 和巨噬细胞炎症和焦亡。动脉粥样硬化患者中 HCC-1 表达增加，HCC-1 过表达通过增强单核细胞募集、M1 加速动脉粥样硬化负荷EC 和巨噬细胞中的极化和焦亡。我们的研究结果表明，HCC-1可以作为诊断动脉粥样硬化的早期生物标志物，能够反映狭窄程度。

HCC-1 (hemofiltrate CC chemokine-1), a CC-type chemokine, exerts function to change intracellular calcium concentration, induce leukocyte, and manipulate enzyme release especially in monocytes. It has been reported that HCC-1 could predict the persistent acute kidney injury or suppress hepatocellular carcinoma by modulating cell cycle and promoting apoptosis, while the effect of HCC-1 on atherosclerosis is poorly understood. Here, we aimed to clarify the function and mechanism of HCC-1 in atherosclerosis and whether it could serve as a novel biomarker for the diagnosis of atherosclerosis.HCC-1 expression in serum, atherosclerotic plaques, and normal arterial tissue from patients with atherosclerosis and control group was assessed by ELISA, immunohistochemistry and confocal microscope, and bioinformatic analysis. The atherosclerotic model of HCC-1 overexpressing and control mice was generated by tail vein injection of adeno-associated virus serotype 9-HCC-1 on an ApoE-/- background. Cell adhesion, polarization, and pyroptosis were evaluated in vitro. The relationship between HCC-1 concentration in serum and atherosclerosis was analyzed in patients with atherosclerosis.HCC-1 expression was positively correlated with the occurrence and stable-unstable switch of atherosclerosis under bioinformatic analysis, which is further supported by the results of increased HCC-1 expression in AS patients both in serum and atherosclerotic plaque. adeno-associated virus serotype 9-HCC-1 mice had higher levels of inflammatory factors, increased macrophage accumulation and pyroptotic rate in plaque, and decreased atherosclerotic plaque stability. In vitro, HCC-1 promoted monocyte adhesion and M1 polarization and induced inflammation and pyroptosis both in ECs and macrophages.HCC-1 expression was increased in patients with atherosclerosis, and HCC-1 overexpression accelerated atherosclerotic burden via an enhancement in monocyte recruitment, M1 polarization, and pyroptosis both in ECs and macrophages. Our findings suggested that HCC-1 may serve as an early biomarker for the diagnosis of atherosclerosis, with the capacity to reflect the degree of stenosis.