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正常人的心脏节律源于右心房的天然起搏点(pacemaker)——窦房结。窦房结的功能异常或者房室传导阻滞会导致心率异常(如心律缓慢)。治疗严重的心动过缓需要植入在技术上已经相当成熟的电子起搏器,但这种治疗存在一些缺陷和不足。近年来,在动物实验模型中应用基因或细胞来重建心脏的生物起搏点已经取得了进展。超极化活化环核苷酸门控(hyperpolarization-activated cyclic-nucleotide-modulated,HCN)通道(起搏通道)通过超极化活化的阳离子电流(hyperpolarization-activated cation current,If)调制心脏的自律性。利用病毒载体或转染HCN基因的细胞将HCN基因导入动物心脏内可重建生物起搏点。也有导入其它基因或植入自律细胞来探索心脏起搏点的重建。本文总结了重建心脏生物起搏点的一些研究进展。一旦稳定性和寿命等关键问题得到相应解决,遗传工程改造的生物起搏点可用于治疗严重的心动过缓。
Normal heart rhythm comes from the natural pacemaker of the right atrium - the sinus node. Sinus node dysfunction or atrioventricular block can lead to abnormal heart rate (such as slow heart rate). Severe bradycardia requires implantation of a technically sophisticated electronic pacemaker, but there are some drawbacks and deficiencies in this treatment. In recent years, progress has been made in the application of genes or cells in animal experimental models to reconstruct biological pacemakers of the heart. Hyperpolarization-activated cyclic-nucleotide-modulated (pNOS) channels (pacing channels) modulate cardiac autonomic by hyperpolarization-activated cation current (If) . The use of viral vectors or cells transfected with the HCN gene to introduce HCN genes into the animal’s heart regenerates biological pacemakers. There are also other genes introduced or autologous cells implanted to explore the reconstruction of cardiac pacemakers. This article summarizes some advances in the reconstruction of cardiac pacemaker. Once critical issues such as stability and longevity are resolved, genetically engineered biological pacemakers can be used to treat severe bradycardia.