The proprotein convertase subtilisin/kexin type 9 (PCSK9) acts via a canonical pathway to regulate circulating low-density lipoprotein-cholesterol (LDL-C) via degradation of the LDL receptor (LDLR) on the liver cell surface. Published research has shown that PCSK9 is involved in atherosclerosis via a variety of non-classical mechanisms that involve lysosomal, inflammatory, apoptotic, mitochondrial, and immune pathways. In this review paper, we summarized these additional mechanisms and described how anti-PCSK9 therapy exerts effects through these mechanisms. These additional pathways further illustrate the regulatory role of PCSK9 in atherosclerosis and offer an in-depth interpretation of how the PCSK9 inhibitor exerts effects on the treatment of atherosclerosis.

中文翻译：

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糖尿病患者与非糖尿病患者中PCSK9替代性非经典机制的研究进展。

前蛋白转化酶枯草杆菌蛋白酶/ kexin 9型（PCSK9）通过规范途径起作用，通过肝细胞表面LDL受体（LDLR）的降解来调节循环中的低密度脂蛋白胆固醇（LDL-C）。已发表的研究表明，PCSK9通过多种非经典机制参与动脉粥样硬化，这些机制涉及溶酶体，炎性，凋亡，线粒体和免疫途径。在这篇综述文章中，我们总结了这些额外的机制，并描述了抗PCSK9治疗如何通过这些机制发挥作用。这些额外的途径进一步说明了PCSK9在动脉粥样硬化中的调节作用，并提供了PCSK9抑制剂如何对动脉粥样硬化的治疗产生作用的深入解释。