Hcy、hs-CRP和CysC与颈动脉粥样硬化的相关性研究进展

Research Progress on the Correlation between Hcy, hs-CRP, CysC and Carotid Atherosclerosis

摘要: 在过去的几十年中，基础和临床研究积累的证据一致表明，炎症参与了颈动脉粥样硬化(Carotid Atherosclerosis, CAS)的发生发展过程，并在其中发挥着关键而复杂的作用。值得思考的是，伴随着相关炎症因子水平的增加，同时也预示着心血管事件发生率的升高。高敏C反应蛋白(High-Sensitivity C-Reactive protein, hs-CRP)是一种非特异性炎性细胞因子，通过增加炎症细胞浸润、增加氧化应激以及损害血管内皮的功能，hs-CRP加速动脉粥样硬化斑块的形成和破坏。同样，同型半胱胺酸(Homocysteine, Hcy)能够参与多机制的血管内皮功能受损，同时刺激血管平滑肌细胞增生，内皮细胞能够调节血管张力、通透性、炎症和细胞生长，在维持血管壁稳态方面起着关键作用。Hcy诱导的血管损伤结局最终影响了血流通路。以及酰化反应导致血栓、颈动脉粥样硬化的产生。然而，血清胱抑素C (Cystatin C, CysC) CysC作为半胱氨酸蛋白酶的抑制剂，在动脉粥样硬化的发病机制中起着重要作用。高水平的胱抑素C可能通过调节蛋白水解和抗蛋白水解活性的平衡直接影响血管壁重塑的过程。以及，胱抑素C可能具有直接的毒性作用，导致其与中风和其他心血管事件的风险相关联。

Abstract: In the past decades, the evidence accumulated from basic and clinical research has consistently shown that inflammation is involved in the occurrence and development of carotid atherosclerosis, and plays a key and complex role in it. It is worth considering that the increase in levels of related inflammatory factors also indicates an increase in the incidence of cardiovascular events. High sen-sitivity C-reactive protein (hs-CRP) is a non-specific inflammatory cytokine. By increasing inflam-matory cell infiltration, increasing oxidative stress and damaging the function of vascular endothe-lium, hs-CRP accelerates the formation and destruction of atherosclerotic plaque. Similarly, homo-cysteine (Hcy) can participate in multiple mechanisms of impaired endothelial function and stimu-late the proliferation of vascular smooth muscle cells. Endothelial cells can regulate vascular ten-sion, permeability, inflammation, and cell growth, playing a crucial role in maintaining vascular wall homeostasis. The outcome of Hcy induced vascular injury ultimately affects the blood flow pathway. And acylation reaction leads to thrombosis and carotid atherosclerosis. However, serum cystatin C (CysC) CysC, as an inhibitor of cysteine protease, plays an important role in the pathogenesis of ath-erosclerosis. High levels of cystatin C may directly affect the process of vascular wall remodeling by regulating the balance between protein hydrolysis and anti protein hydrolysis activity. Moreover, cystatin C may have direct toxic effects, leading to its association with the risk of stroke and other cardiovascular events.