Dong Caijuan, Wang Ya, Ma Aiqun, Wang Tingzhong
Department of Cardiovascular Medicine, First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, China.
Key Laboratory of Molecular Cardiology, Shaanxi Province, Xi'an, China.
Front Physiol. 2020 Dec 17;11:609733. doi: 10.3389/fphys.2020.609733. eCollection 2020.
Cardiac voltage-gated sodium channel Na1.5, encoded by , is crucial for the upstroke of action potential and excitation of cardiomyocytes. Na1.5 undergoes complex processes before it reaches the target membrane microdomains and performs normal functions. A variety of protein partners are needed to achieve the balance between transcription and mRNA decay, endoplasmic reticulum retention and export, Golgi apparatus retention and export, selective anchoring and degradation, activation, and inactivation of sodium currents. Subtle alterations can impair Na1.5 in terms of expression or function, eventually leading to Na1.5-associated diseases such as lethal arrhythmias and cardiomyopathy.
由[基因名称]编码的心脏电压门控钠通道Na1.5，对于动作电位的上升支和心肌细胞的兴奋至关重要。Na1.5在到达靶膜微区并执行正常功能之前会经历复杂的过程。需要多种蛋白质伴侣来实现转录与mRNA降解、内质网滞留与输出、高尔基体滞留与输出、选择性锚定与降解、钠电流的激活与失活之间的平衡。细微的改变可能在表达或功能方面损害Na1.5，最终导致与Na1.5相关的疾病，如致命性心律失常和心肌病。
