Beyond mechanical revascularization: thrombo-inflammatory mechanisms and vascular bed-specific design of intracranial stents.

Cerebrovascular and coronary artery diseases are among the leading causes of mortality. Stent systems are widely used in both cardiac and cerebrovascular interventions; however, in-stent restenosis and acute stent thrombosis associated with bare-metal stents can cause severe ischemic complications and markedly reduce therapeutic efficacy. Although drug-eluting stents significantly decrease the incidence of restenosis, they carry an increased risk of late and very late stent thrombosis. Currently, antiplatelet therapy remains the primary strategy to prevent stent-related thrombosis. Nevertheless, drugs eluted from stents can impair endothelial recovery. This delay in reendothelialization increases the risk of late thrombotic events. Therefore, a comprehensive understanding of the mechanisms underlying stent implantation-associated pathology is essential for the development of next-generation stent platforms and targeted pharmacological strategies. In this review, we systematically discuss the pathological mechanisms underlying stent-associated complications from four key perspectives: endothelial cells, vascular smooth muscle cells, the coagulation system, and inflammatory responses. By integrating current evidence from both coronary and intracranial vascular systems, this review aims to provide mechanistic insights to support the optimization of stent design and improve long-term clinical outcomes.