摘要
Cardiac arrhythmias are among the most common causes of death in the world. Foundational studies established the critical role of ion channel disorders in arrhythmias, yet defects in ion channels themselves, such as mutations, may not account for all arrhythmias. Despite the progress made in recent decades, the antiarrhythmic drugs currently available have limited effectiveness,and the majority of these drugs can have proarrhythmic effects. This review describes novel knowledge on cellular mechanisms that cause cardiac arrhythmias, focuses on the dysfunction of subcellular organelles and intracellular logistics, and discusses potential strategies and challenges for developing novel, safe and effective treatments for arrhythmias.
Cardiac arrhythmias are among the most common causes of death in the world. Foundational studies established the critical role of ion channel disorders in arrhythmias, yet defects in ion channels themselves, such as mutations, may not account for all arrhythmias. Despite the progress made in recent decades, the antiarrhythmic drugs currently available have limited effectiveness,and the majority of these drugs can have proarrhythmic effects. This review describes novel knowledge on cellular mechanisms that cause cardiac arrhythmias, focuses on the dysfunction of subcellular organelles and intracellular logistics, and discusses potential strategies and challenges for developing novel, safe and effective treatments for arrhythmias.
基金
supported by the National Key Basic Research Program of China (2013CB531100 to Yi-Han Chen)
the Major International Joint Research Program of China (81120108004 to Yi-Han Chen)
the Key Program of National Natural Science Foundation of China (81530017 to Yi-Han Chen)
the National Innovative Research Groups Program of the National Natural Science Foundation of China (81221001 to Yi-Han Chen)
the General Program of National Natural Science Foundation of China (81170224, 81270313 to Jun Li, 31271214 to Yi-Han Chen)
the National Natural Science Foundation of China (81670295 to Li Lin)