Human TK gene transfer has been pro

已证明人类TK基因转移可减轻球囊导管诱导的新内膜形成。HUK是<br><br>人体内的传统知识，通常用于预防缺血再灌注损伤。在本实验中，我们观察到HUK通过减少VSMC，下调TGF-b1的表达和Smad2 / 3的磷酸化并同时增加eNOS的活性来抑制球囊损伤的颈动脉内膜增生。<br>自1980年代问世以来，PTAS已成为治疗动脉粥样硬化狭窄，预防心肌梗塞和缺血性中风的流行方法。PTAS术后支架内再狭窄显着限制了支架置入术后的长期预后。活化的巨噬细胞的黏附和侵袭，VSMC的迁移和增殖以及炎症因子和细胞因子的表达增强会导致血管重塑和内膜增生。因此，抑制巨噬细胞浸润以及VSMC迁移和增殖是PTAS后动脉粥样硬化和再狭窄的可行治疗策略。

Human TK gene transfer has been proved to attenuate neointima formation induced by balloon catheter. HUK is<br><br>a TK in the human body and is usually administered to pre- vent ischemia-reperfusion injury. In the present experi- ment, we observed that HUK had an inhibitory effect on intimal hyperplasia of balloon-injured carotid artery by reducing VSMCs, downregulating the expression of TGF-b1 and phosphorylation of Smad2/3, and meanwhile increasing the activities of eNOS.<br>Since the 1980s, when it was introduced, PTAS has become a popular method to treat atherosclerotic stenosis and to prevent myocardial infarction and ischemic stroke. In-stent restenosis after PTAS significantly limits the long- term prognosis after stenting. The adhesion and invasion of activated macrophages, migration and proliferation of VSMCs, and enhanced expression of inflammatory factors and cytokines cause vascular remodeling and intimal hyper- plasia. Hence, inhibition of macrophage infiltration and VSMC migration and proliferation is a feasible therapeutic strategy for atherosclerosis and restenosis after PTAS.

人类TK基因转移已被证明可以减轻球囊导管诱导的新生内膜形成。胡克是<br>在人体内的一种TK，通常用于预防缺血再灌注损伤。在本实验中，我们观察到HUK通过减少血管平滑肌细胞，下调TGF-b1的表达和Smad2/3的磷酸化，同时增加eNOS的活性来抑制球囊损伤颈动脉内膜增生。<br>自20世纪80年代引入PTAS以来，PTAS已成为治疗动脉粥样硬化性狭窄、预防心肌梗死和缺血性中风的常用方法。经皮冠状动脉成形术后支架内再狭窄显著限制支架置入术后的长期预后。活化巨噬细胞的粘附和侵袭，血管平滑肌细胞的迁移和增殖，以及刺激因子和细胞因子表达的增强，导致血管重塑和内膜增生。因此，抑制巨噬细胞的增殖和迁移是治疗PTAS后动脉粥样硬化和再狭窄的一种可行的治疗策略。