Tunicamycin Attenuates Cardiac Automaticity by Reducing HCN Current

Tunicamycin (TM), as a natural inhibitor of N-linked glycosylation in eukaryotes, can promote apoptosis and sensitize cancer cells to chemotherapy and radiation therapy in numerous studies. The cardiotoxicity of anticarcinogen always deserved serious consideration. Although the promising anticancer effect of TM is exhilarating, more cardiac adverse reactions are remaining needed to identify and explore. Herein, we focus on the electrophysiological aberration after TM application, and unforeseen found that sinus bradycardia is almost the one and only arrhythmia induced by TM. It implies that the impairment of cardiac pacemaker function should be noticed in the adverse cardiac effect of TM. Furthermore, we found that the TM treatment significantly reduced neonatal cardiomyocytes' automaticity, and diminished. If regulating the cardiac automatic action potential. The current findings illustrate the TM antiarrhythmic mechanism, which might be useful for developing N-glycosylation inhibitor anticarcinogen.