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Updated: May 15, 2026
A Murine Model of Stent Implantation in the Carotid Artery for the Study of Restenosis
Published on: May 14, 2013
Beyond mechanical revascularization: thrombo-inflammatory mechanisms and vascular bed-specific design of intracranial
Yingjun Liu1,2,3,4,5, Jinquan Li1,2,3,4,5, Liuxun Hu1,2,3,4,5
1Department of Neurosurgery, Huashan Hospital, Shanghai Medical College, Fudan University, Shanghai, China.
Insights
Understanding stent complications is key to improving cardiovascular and cerebrovascular treatments. This review details how endothelial cells, smooth muscle cells, coagulation, and inflammation impact stent performance, guiding future device and drug development.
Area of Science:
- Cardiovascular research
- Vascular biology
- Medical device technology
Background:
- Cerebrovascular and coronary artery diseases are leading causes of mortality.
- Stent systems are crucial for treating these conditions but are associated with complications like in-stent restenosis and thrombosis.
- Bare-metal stents and drug-eluting stents present distinct challenges, including ischemic events and stent thrombosis, necessitating improved strategies.
Purpose of the Study:
- To systematically review the pathological mechanisms underlying stent implantation-associated complications.
- To provide mechanistic insights into endothelial cells, vascular smooth muscle cells, coagulation, and inflammatory responses.
- To inform the development of next-generation stent platforms and targeted pharmacological strategies for improved clinical outcomes.
Main Methods:
- Systematic review of pathological mechanisms.
- Integration of evidence from coronary and intracranial vascular systems.
- Analysis of cellular and systemic responses to stent implantation.
Main Results:
- Stent-associated complications arise from complex interactions involving endothelial dysfunction, vascular smooth muscle cell proliferation, coagulation system activation, and inflammatory responses.
- Drug-eluting stents, while reducing restenosis, can impede endothelial recovery, increasing late thrombotic risks.
- Bare-metal stents are linked to acute thrombosis and restenosis, highlighting the need for balanced therapeutic approaches.
Conclusions:
- A comprehensive understanding of stent-associated pathology is essential for advancing cardiovascular and cerebrovascular interventions.
- Optimizing stent design and developing targeted pharmacological strategies require a deep insight into the interplay of cellular and systemic factors.
- Future research should focus on enhancing reendothelialization and mitigating thrombotic risks for improved long-term patient outcomes.
Abstract:
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.
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