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<p>Arrhythmias, driven by abnormal electrical activity and structural remodeling, are a leading cause of cardiovascular mortality. Despite advances in treatment methods, therapeutic limitations persist due to an incomplete understanding of the heterogeneous mechanisms involved. The phosphoinositide 3-kinase/protein kinase B (PI3K/AKT) signaling pathway, a central regulator of cellular survival, metabolism, and electrophysiology, has been identified as a key factor in arrhythmia development. This review summarises evidence indicating that dysregulated PI3K/AKT signaling promotes arrhythmias via four interconnected pathways: electrophysiological remodeling, oxidative stress and inflammation, autophagy and apoptosis, and fibrotic structural remodeling. Notably, under certain conditions, the PI3K/AKT signaling pathway exhibits bidirectional regulatory effects. Furthermore, evidence suggests that pharmacologically targeting the PI3K/AKT pathway exhibits significant anti-arrhythmic potential.</p>

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The impact of the PI3K/AKT pathway on arrhythmia: mechanisms of action and therapeutic potential

  • 期刊论文

  • 发表日期：

    2026年1月23日

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  • Tao Leng,
  • Jue Zhao,
  • Zuo Xiao,
  • Siqi Hao,
  • Wen Xie,
  • Qian Nie

摘要

Arrhythmias, driven by abnormal electrical activity and structural remodeling, are a leading cause of cardiovascular mortality. Despite advances in treatment methods, therapeutic limitations persist due to an incomplete understanding of the heterogeneous mechanisms involved. The phosphoinositide 3-kinase/protein kinase B (PI3K/AKT) signaling pathway, a central regulator of cellular survival, metabolism, and electrophysiology, has been identified as a key factor in arrhythmia development. This review summarises evidence indicating that dysregulated PI3K/AKT signaling promotes arrhythmias via four interconnected pathways: electrophysiological remodeling, oxidative stress and inflammation, autophagy and apoptosis, and fibrotic structural remodeling. Notably, under certain conditions, the PI3K/AKT signaling pathway exhibits bidirectional regulatory effects. Furthermore, evidence suggests that pharmacologically targeting the PI3K/AKT pathway exhibits significant anti-arrhythmic potential.