Institute of Cardiovascular Disease, Key Laboratory for Arteriosclerology of Hunan Province, Hunan International Scientific and Technological Cooperation Base of Arteriosclerotic Disease, University of South China, Hengyang, Hunan 421001, PR China.
Hunan Environmental Biology Vocational and Technical College, Hengyang, Hunan 421001, PR China.
Clin Chim Acta. 2019 Aug;495:358-364. doi: 10.1016/j.cca.2019.05.005. Epub 2019 May 7.
Proprotein convertase subtilisin kexin 9 (PCSK9) regulates lipid metabolism by degrading low-density lipoprotein receptor on the surface of hepatocytes. PCSK9-mediated lipid degradation is associated with lipophagy. Lipophagy is a process by which autophagosomes selectively sequester lipid-droplet-stored lipids and are delivered to lysosomes for degradation. Lipophagy was first discovered in hepatocytes, and its occurrence provides important fundamental insights into how lipid metabolism regulates cellular physiology and pathophysiology. Furthermore, PCSK9 may regulate lipid levels by affecting lipophagy. This review will discuss recent advances by which PCSK9 mediates lipid degradation via the lipophagy pathway and present lipophagy as a potential therapeutic target for atherosclerosis.
前蛋白转化酶枯草溶菌素 9(PCSK9)通过降解肝细胞表面的低密度脂蛋白受体来调节脂质代谢。PCSK9 介导的脂质降解与脂噬作用有关。脂噬作用是一种自噬体选择性隔离储存于脂滴中的脂质并将其递送至溶酶体进行降解的过程。脂噬作用最初在肝细胞中被发现,其发生为脂质代谢如何调节细胞生理学和病理生理学提供了重要的基本见解。此外,PCSK9 可能通过影响脂噬作用来调节脂质水平。本综述将讨论 PCSK9 通过脂噬作用途径介导脂质降解的最新进展,并将脂噬作用作为动脉粥样硬化的潜在治疗靶点进行介绍。