O' Brien Edward R, Ma Xiaoli, Simard Trevor, Pourdjabbar Ali, Hibbert Benjamin
Division of Cardiology, University of Ottawa Heart Institute, Ontario, Canada.
Cardiovasc Hematol Disord Drug Targets. 2011 Mar 1;11(1):30-9. doi: 10.2174/187152911795945169.
Revascularization remains the cornerstone of managing obstructive coronary artery disease. Although percutaneous coronary interventions involving the insertion of metal scaffolds, known as stents, has emerged as the preferred method of restoring vessel patency, as many as 30% of patients will experience a gradual re-narrowing of the lumen caused by neointima (NI) formation, resulting in a condition known as in-stent restenosis (ISR). ISR represents a significant limitation to percutaneous revascularization - however, abrogating NI formation following stent implantation has been hampered by an incomplete understanding of the pathogenesis of in-stent lesions. While numerous mechanisms have been proposed to explain the pathogenesis of ISR, data from human and animal models have yielded conflicting results. Herein, we review key studies of NI development following vascular injury with a focus on the origin of cells participating in NI formation.
血管重建仍然是治疗阻塞性冠状动脉疾病的基石。尽管涉及插入金属支架（即支架）的经皮冠状动脉介入治疗已成为恢复血管通畅的首选方法，但多达30%的患者会因新生内膜（NI）形成而出现管腔逐渐再狭窄，导致支架内再狭窄（ISR）。ISR是经皮血管重建的一个重大限制——然而，由于对支架内病变发病机制的理解不完整，支架植入后抑制NI形成受到了阻碍。虽然已经提出了许多机制来解释ISR的发病机制，但来自人类和动物模型的数据却产生了相互矛盾的结果。在此，我们回顾了血管损伤后NI发展的关键研究，重点关注参与NI形成的细胞来源。
