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.
CITATION STYLE
Tang, Y., Li, S. L., Hu, J. H., Sun, K. J., Liu, L. L., & Xu, D. Y. (2020, March 13). Research progress on alternative non-classical mechanisms of PCSK9 in atherosclerosis in patients with and without diabetes. Cardiovascular Diabetology. BioMed Central Ltd. https://doi.org/10.1186/s12933-020-01009-4
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