Exenatide reduces atrial fibrillation susceptibility by inhibiting hKv1.5 and hNav1.5 channels

Exenatide, a promising cardioprotective agent, protects against cardiac structural remodeling and diastolic dysfunction. Combined blockade of sodium and potassium channels is valuable for managing atrial fibrillation (AF). Here, we explored whether exenatide displayed anti-AF effects by inhibiting h...

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Veröffentlicht in:	The Journal of biological chemistry 2024-05, Vol.300 (5), p.107294-107294, Article 107294
Hauptverfasser:	Zhou, Qian, Hao, Guoliang, Xie, Wensen, Chen, Bin, Lu, Wuguang, Wang, Gongxin, Zhong, Rongling, Chen, Jiao, Ye, Juan, Shen, Jianping, Cao, Peng
Format:	Artikel
Sprache:	eng
Schlagworte:	Action Potentials - drug effects Animals atrial fibrillation Atrial Fibrillation - drug therapy Atrial Fibrillation - metabolism close channel block exenatide Exenatide - pharmacology Exenatide - therapeutic use HEK293 Cells hKv1.5 hNav1.5 Humans Kv1.5 Potassium Channel - antagonists & inhibitors Male Myocytes, Cardiac - drug effects Myocytes, Cardiac - metabolism NAV1.5 Voltage-Gated Sodium Channel - genetics NAV1.5 Voltage-Gated Sodium Channel - metabolism open channel block Rats Rats, Sprague-Dawley Voltage-Gated Sodium Channel Blockers - pharmacology Voltage-Gated Sodium Channel Blockers - therapeutic use
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