Study of PCSK9 in acute coronary syndrome

The incidence of acute coronary syndrome (ACS) is increasing year by year in our country. The patients with ACS not only need to receive dual antiplatelet therapy for at least 12 months, but also to undergo intensive lipid-lowering treatment (LDL-C<1.4 mmol/L). Recently, many studies have shown that the proprotein convertase subtilisin-kexin type 9 (PCSK9) mainly secreted by liver cells can bind to low density lipoprotein receptor (LDLR) on liver cell surface in a non-enzymatic manner and eventually leads to high LDL-C levels. In addition, PCSK9 from plasma and vascular cells can promote platelet activation, leukocyte recruitment and clot formation, which increases the risk of atherosclerotic plaque and ACS. PCSK9 inhibitors (proprotein convertase subtilisin-kexin type 9 inhibitor, PCSK9I), as emerging therapeutic targets, can rapidly reduce low-density lipoprotein cholesterol with fewer adverse effects. Therefore, this review describes the recent research progress in the physiological mechanism of PCSK9 with ACS and the latest therapeutic mechanisms and clinical applications of PCSK9I to provide literature support for further study of disease treatment and prognosis.