ArticleActa Cardiologica Sinica2026
PCSK9 Inhibitor Attenuates Platelet TLR4 in ACS and TLR4 Blockers Prevent PCSK9-Mediated Platelet Activation.
Article in Acta Cardiologica Sinica, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Background: Proprotein convertase subtilisin/kexin type 9 (PCSK9) regulates platelet activation through multiple signaling pathways. This study aimed to determine whether PCSK9 modulates platelet activation via Toll-like receptor 4 (TLR4). Methods: A total of 120 patients with acute coronary syndrome (ACS) were divided into a control group and an experimental group receiving subcutaneous evolocumab. Platelet surface TLR4 was quantified by flow cytometry. Platelet-rich plasma from healthy volunteers (n = 5) was incubated with normal saline, PCSK9, PCSK9 + evolocumab, or PCSK9 + the TLR4 inhibitor resatorvid (TAK-242). Platelets were then stimulated with adenosine diphosphate, and aggregation was measured. Plasma thromboxane A2 (TXA2) was measured by ELISA. Megakaryoblastic leukemia cells (MEG-01) were co-incubated with PCSK9 and stained for TLR4 and PCSK9 by immunofluorescence. Results: PCSK9 significantly enhanced platelet aggregation and TXA2 release in vitro; both effects were abolished by evolocumab and TAK-242. In ACS patients, evolocumab treatment reduced platelet surface TLR4 expression and decreased plasma TXA2 levels. Dual immunofluorescence staining demonstrated co-localization of TLR4 and PCSK9 in MEG-01 cells. Conclusions: This study provides the first evidence that PCSK9 inhibitors downregulate platelet TLR4 expression in ACS patients. The pro-aggregatory effects of PCSK9 on platelets were counteracted by TLR4 inhibition, indicating a mechanistic link between PCSK9 and TLR4 signaling in platelet activation. Co-localization of TLR4 and PCSK9 in MEG-01 cells supports a potential interaction between the two proteins.
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