Mitra A K, Agrawal D K
Departments of Biomedical Sciences, Medicine, and Medical Microbiology and Immunology, Creighton University School of Medicine, Omaha, NE 68178, USA.
J Clin Pathol. 2006 Mar;59(3):232-9. doi: 10.1136/jcp.2005.025742.
The long term outcome of stent implantation is affected by a process called in stent restenosis (ISR). Multiple contributory factors have been identified, but clear understanding of the overall underlying mechanism remains an enigma. ISR progresses through several different phases and involves numerous cellular and molecular constituents. Platelets and macrophages play a central role via vascular smooth muscle cell migration and proliferation in the intima to produce neointimal hyperplasia, which is pathognomic of ISR. Increased extracellular matrix formation appears to form the bulk of the neointimal hyperplasia tissue. Emerging evidence of the role of inflammatory cytokines and suppressors of cytokine signalling make this an exciting and novel field of antirestenosis research. Activation of Akt pathway triggered by mechanical stretch may also be a contributory factor to ISR formation. Prevention of ISR appears to be a multipronged attack as no therapeutic "magic bullet" exists to block all the processes in one go.
支架植入的长期结果受一种称为支架内再狭窄（ISR）的过程影响。已确定了多种促成因素，但对整体潜在机制的清晰理解仍然是个谜。ISR通过几个不同阶段发展，涉及众多细胞和分子成分。血小板和巨噬细胞通过血管平滑肌细胞在内膜中的迁移和增殖发挥核心作用，从而产生内膜增生，这是ISR的病理特征。细胞外基质形成增加似乎构成了内膜增生组织的大部分。炎症细胞因子和细胞因子信号抑制因子作用的新证据使这成为抗再狭窄研究中一个令人兴奋的新领域。机械拉伸触发的Akt通路激活也可能是ISR形成的一个促成因素。由于不存在能一次性阻断所有过程的治疗“神奇子弹”，ISR的预防似乎需要多方面的努力。
