Cardiovascular Development and Disease Genetic Regulation of Sinoatrial Node Development and Pacemaker Program in the Venous Pole
Cardiovascular Development and Disease Genetic Regulation of Sinoatrial Node Development and Pacemaker Program in the Venous Pole
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通讯作者：
Wenduo Ye;Yingnan Song;Zhen Huang;Yanding Zhang;Yiping Chen;R. Poelmann;M. Jongbloed
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作者：
Wenduo Ye;Yingnan Song;Zhen Huang;Yanding Zhang;Yiping Chen;R. Poelmann;M. Jongbloed
永久性窦房结（SAN）是哺乳动物心脏的主要起搏器，由表达Hcn 4和转录因子Shox 2的前起搏胚胎静脉极的一部分发育而来。应注意，源自肺静脉和体静脉回流的心肌袖的异位起搏活动（两者均源自静脉极中的Shox 2+前起搏细胞）引起心房颤动。然而，在胚胎静脉极细胞和SAN的起搏器性能之间的发展联系仍然在很大程度上没有特点。此外，遗传程序的发展异质群体的SAN也是低估。在这里，我们回顾了文献，以更好地了解SAN的发展与静脉窦心肌和肺静脉心肌的异质性。我们还试图重新审视遗传模型的发展起搏器活动的角度Shox2-Nkx2 - 5上位拮抗作用。最后，我们描述了最近的努力破译的监管网络起搏器的发展全基因组的方法。
The definitive sinoatrial node (SAN), the primary pacemaker of the mammalian heart, develops from part of pro-pacemaking embryonic venous pole that expresses both Hcn4 and the transcriptional factor Shox2. It is noted that ectopic pacemaking activities originated from the myocardial sleeves of the pulmonary vein and systemic venous return, both derived from the Shox2 + pro-pacemaking cells in the venous pole, cause atrial fibrillation. However, the developmental link between the pacemaker properties in the embryonic venous pole cells and the SAN remains largely uncharacterized. Furthermore, the genetic program for the development of heterogeneous populations of the SAN is also under-appreciated. Here, we review the literature for a better understanding of the heterogeneous development of the SAN in relation to that of the sinus venosus myocardium and pulmonary vein myocardium. We also attempt to revisit genetic models pertinent to the development of pacemaker activities in the perspective of a Shox2-Nkx2-5 epistatic antagonism. Finally, we describe recent efforts in deciphering the regulatory networks for pacemaker development by genome-wide approaches.