反义治疗抑制再狭窄  

Antisense Strategies to Inhibit Restenosis

作　　者：周俊[1] 戚文航[1] 

机构地区：[1]上海第二医科大学附属瑞金医院心内科，上海200025

出　　处：《心血管病学进展》2003年第5期334-337,共4页Advances in Cardiovascular Diseases

摘　　要：血管再狭窄是心血管治疗领域的热点及难点 ,发生机制包括血管弹性回缩、血栓形成、血管重构和内膜增生。平滑肌细胞增殖、迁移在其病理形成中起关键作用。靶基因的硫代磷酸化寡核苷酸通过杂交依赖反义、G quartetaptameric、非G quartetaptameric和非序列特异性抑制平滑肌细胞增殖、迁移及活体血管新生内膜形成。此外 ,硫代磷酸化寡核苷酸具有免疫调节作用。目前反义治疗多采用局部给药法进行抗再狭窄治疗。新的反义治疗抑制再狭窄策略是采用E2F诱骗寡核苷酸调节平滑肌细胞周期调节基因的表达 。Restenosis after percutaneous transluminal coronary angioplasty(PTCA) remains an important clinical problem,which is a complex,multifactorial process consisting of various degrees of elastic recoil,thrombus formation,vascular remodeling and intimal hyperplasia.Vascular smooth muscle proliferation(SMC) and migration from the arterial wall media into the intima are believed to play a critical role in the pathogenesis of restenosis phosphorothioate(PS) oligodeoxynucleotides targeted against genes inhibit in vitro SMC proliferation and migration and in vivo neointimal formation by hybridization dependent antisense mechanism,G quartet aptameric and non G quartet,non sequence specific inhibitory effects.In addition,PS oligodeoxynucleotides manifest other non sequence specific immunomodulatory effects.At present,much interest has developed in the local administration of anti restenosis therapies.A novel approach to inhibit restenosis has been to target the transcription factor E2F.The intracellular delivery of the E2F decoys effects inhibition of SMC cell cycle regulatory genes and inhibits in vitro SMC proliferation and in vivo neointimal lesion formation.

关 键 词：血管再狭窄 反义治疗 平滑肌细胞 硫代磷酸化寡核苷酸 发生机制 经皮腔内冠状动脉成形术 心血管病 

分 类 号：R541.4[医药卫生—心血管疾病]