钠-葡萄糖协同转运蛋白2抑制剂降低新发房颤潜在机制研究

Potential mechanism of sodium-glucose cotransporter 2 inhibitors in reducing new atrial fibrillation

房颤作为最常见的心律失常,可以单独也可以继发于其他心血管疾病。心房肌细胞离子通道、线粒体功能、能量守恒等的紊乱是房性心律失常发生和维持的细胞机制。钠-葡萄糖协同转运蛋白2抑制剂作为新型降糖药而非抗心律失常药,不仅对心力衰竭有积极影响,还能调节离子通道平衡、改善线粒体功能、维持能量平衡、缓解心房结构重塑,从而潜在地降低新发房颤的发生率。本文对钠-葡萄糖协同转运蛋白2抑制剂降低新发房颤潜在机制进行综述。

Atrial fibrillation, the most common arrhythmia, can occur alone or as a result of other cardiovascular conditions.The disturbances of ion channels, mitochondrial function and energy conservation of atrial myocytes provide the cellular matrix for the occurrence and maintenance of atrial arrhythmias.As a new anti-sugar drug instead of anti-arrhythmic drugs, sodium-glucose cotransporter 2 inhibitors have been shown in several clinical studies to not only improve heart failure but also adjust ion channel balance, improve mitochondrial function, maintain energy balance, and ease atrial structural remodeling, potentially reducing the incidence of new atrial fibrillation.The potential mechanisms by which sodium-glucose cotransporter 2 inhibitors reduce the incidence of new atrial fibrillation are discussed in this article.