CAJ | 학술논문

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.
정상인적심장절률원우우심방적천연기박점(pacemaker)--두방결.두방결적공능이상혹자방실전도조체회도치심솔이상(여심률완만).치료엄중적심동과완수요식입재기술상이경상당성숙적전자기박기,단저충치료존재일사결함화불족.근년래,재동물실험모형중응용기인혹세포래중건심장적생물기박점이경취득료진전.초겁화활화배핵감산문공(hyperpolarization-activated cyclic-nucleotide-modulated,HCN)통도(기박통도)통과초겁화활화적양리자전류(hyperpolarization-activated cation current,If)조제심장적자률성.이용병독재체혹전염HCN기인적세포장HCN기인도입동물심장내가중건생물기박점.야유도입기타기인혹식입자률세포래탐색심장기박점적중건.본문총결료중건심장생물기박점적일사연구진전.일단은정성화수명등관건문제득도상응해결,유전공정개조적생물기박점가용우치료엄중적심동과완.
Normal rhythm in a healthy human heart originates from the natural biological pacemaker, the sinoatrial (SA) node which locates in the right atrium. SA node dysfunction or atrial-ventricular (AV) conduction block causes improper heart rate (bradycardia).Such dysfunction, if severe enough, is currently treated by implanting an electronic pacemaker which has been well established technically, but there are some limitations and inadequacies. Recently, progress in developing engineered cardiac biopacemakers with use of genes or cells has been made in experimental animal models. The hyperpolarization-activated cyclic-nucleotide-modulated(HCN) channel (pacemaker channel) modulates cardiac automaticity via the hyperpolarization-activated cation current (If). HCN genes have been delivered to animal myocardium via viral vectors or HCN-transferred cells for recreating biological pacemakers. Approaches with non-HCN genes or transplantation of beating cells are also novel and have been investigated for generating cardiac biopacers. This article summarizes the progresses in research on recreation of cardiac biopacemakers. Genetically engineered biological pacemaker holds great promise to potentially cure severe bradycardia if critical issues, such as their stability and longevity, are properly solved.