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Abstract：
This study aims to investigate the mechanism of platelet activation-induced thrombosis in patients with acute non-ST segment elevation myocardial infarction (NSTEMI) by detecting the expression of autophagy-associated proteins in platelets of patients with NSTEMI. A prospective study was conducted on 121 patients with NSTEMI who underwent emergency coronary angiography and optical coherence tomography. The participants were divided into two groups: the ST segment un-offset group (n = 64) and the ST segment depression group (n = 57). We selected a control group of 60 patients without AMI during the same period. The levels of autophagy-associated proteins and the expression of autophagy-associated proteins in platelets were measured using immunofluorescence staining and Western blot. In NSTEMI, the prevalence of red thrombus was higher in the ST segment un-offset myocardial infarction (STUMI) group, whereas white thrombus was more common in the ST segment depression myocardial infarction (STDMI) group. Furthermore, the platelet aggregation rate was significantly higher in the white thrombus group compared with the red thrombus group. Compared with the control group, the autophagy-related protein expression decreased, and the expression of αIIbβ3 increased in NSTEMI. The overexpression of Beclin1 could activate platelet autophagy and inhibit the expression of αIIbβ3. The results suggested that the increase in platelet aggregation rate in patients with NSTEMI may be potentially related to the change in autophagy. And the overexpression of Beclin1 could reduce the platelet aggregation rate by activating platelet autophagy. Our findings demonstrated that Beclin1 could be a potential therapeutic target for inhibiting platelet aggregation in NSTEMI.
摘要：
本研究通过检测急性非ST段抬高型心肌梗死(NSTEMI)患者血小板中自噬相关蛋白的表达,探讨NSTEMI患者血小板活化诱导血栓形成的机制。对121例接受急诊冠状动脉造影和光学相干断层扫描的NSTEMI患者进行了前瞻性研究。将参与者分为两组：ST段未偏移组（n=64）和ST段凹陷组（n=57）。我们选择同期没有AMI的60例患者作为对照组。采用免疫荧光染色和Westernblot检测血小板中自噬相关蛋白和自噬相关蛋白的表达。在NSTEMI,红色血栓的患病率在ST段未抵消心肌梗死（STUMI）组中较高，而白色血栓在ST段压低心肌梗死（STdmi）组中更为常见。此外，白色血栓组的血小板聚集率明显高于红色血栓组。与对照组相比,自噬相关蛋白表达降低,NSTEMI中αIIbβ3的表达增加。Beclin1的过表达可激活血小板自噬并抑制αIIbβ3的表达。结果提示NSTEMI患者血小板聚集率的升高可能与自噬的改变有关。Beclin1过表达可通过激活血小板自噬降低血小板聚集率。我们的发现表明Beclin1可能是抑制NSTEMI血小板聚集的潜在治疗靶点。
