靶向三重奏:C型凝集素样受体2、糖蛋白VI与血小板内皮细胞黏附分子-1作为急性缺血性脑卒中血栓形成与神经炎症的调节靶点OA

Acute ischemic stroke(AIS)is a kind of neurological disease caused by impaired cerebral blood supply due to various etiologies,resulting in ischemic-hypoxic necrosis of brain tissue and subsequent brain dysfunction.The current reperfusion therapy for AIS faces challenges including a short treatment window and bleeding risks.Research indicates that this neurological disorder may originate from cerebral thrombotic vascular occlusion,with the intrinsic connection between thrombi and pro-inflammatory processes,which provides critical mechanisms for AIS occurrence.Key therapeutic factors in AIS management include C-type lectin-like receptor 2(CLEC-2),glycoprotein VI(GPVI),and platelet endothelial cell adhesion molecule-1(PECAM1),which are promising due to their crucial roles in thrombosis-inflammation crosstalk.However,several key issues remain to be addressed-① Insufficient research depth:The specific mechanisms of CLEC-2,GPVI,and PECAM1 in AIS pathogenesis require systematic elucidation,particularly regarding integration with modern pathophysiological frameworks.② Clinical study standardization gaps:Most trials are limited by small sample sizes and lack standardized protocols,limiting result reliability and reproducibility.Future efforts should focus on investigating receptor mechanisms during hypoxia,identifying key kinases that regulate PECAM1's pro-inflammatory functions,developing inhibitors that effectively target GPVI and CLEC-2 while enhancing PECAM1-mediated vascular protection,and establishing scientific patient stratification systems.Dynamic monitoring of sGPVI and sPECAM1 concentrations could help precisely identify high-risk patients for thrombotic and inflammatory responses,thereby enabling the creation of targeted drug delivery systems to provide more accurate clinical guidance.