Chloride channel 3 (ClC-3), a Cl⁻/H⁺ antiporter, has been well established as a member of volume-regulated chloride channels (VRCCs). ClC-3 may be a crucial mediator for activating inflammation-associated signaling pathways by regulating protein phosphorylation. A growing number of studies have indicated that ClC-3 overexpression plays a crucial role in mediating increased plasma low-density lipoprotein levels, vascular endothelium dysfunction, pro-inflammatory activation of macrophages, hyper-proliferation and hyper-migration of vascular smooth muscle cells (VSMCs), as well as oxidative stress and foam cell formation, which are the main factors responsible for atherosclerotic plaque formation in the arterial wall. In the present review, we summarize the molecular structures and classical functions of ClC-3. We further discuss its emerging role in the atherosclerotic process. In conclusion, we explore the potential role of ClC-3 as a therapeutic target for atherosclerosis.

氯化物通道 3 (ClC-3)，a Cl ^- /H ⁺反转运蛋白已被公认为体积调节氯离子通道 (VRCCs) 的成员。ClC-3 可能是通过调节蛋白质磷酸化激活炎症相关信号通路的关键介质。越来越多的研究表明，ClC-3 过表达在介导血浆低密度脂蛋白水平升高、血管内皮功能障碍、巨噬细胞的促炎激活、血管平滑肌细胞的过度增殖和过度迁移中起关键作用。 VSMCs)，以及氧化应激和泡沫细胞形成，它们是导致动脉壁中动脉粥样硬化斑块形成的主要因素。在本综述中，我们总结了 ClC-3 的分子结构和经典功能。我们进一步讨论了它在动脉粥样硬化过程中的新兴作用。