Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, 250021, China.
Department of Cardiology, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, 250021, China.
Hum Cell. 2024 Nov 6;38(1):14. doi: 10.1007/s13577-024-01145-z.
The development of atrial fibrillation (AF) is a highly complex, multifactorial process involving pathophysiologic mechanisms, molecular pathway mechanisms and numerous genetic abnormalities. The pathophysiologic mechanisms including altered ion channels, abnormalities of the autonomic nervous system, inflammation, and abnormalities in Ca2 + handling. Molecular pathway mechanisms including, but not limited to, renin-angiotensin-aldosterone (RAAS), transforming growth factor-β (TGF-β), oxidative stress (OS). Although in clinical practice, the distinction between types of AF such as paroxysmal and persistent determines the choice of treatment options. However, it is the pathophysiologic alterations present in AF that truly determine the success of AF treatment and prognosis, but even more so the molecular mechanisms and genetic alterations that lie behind them. One tiny clue reveals the general trend, and small beginnings show how things will develop. This article will organize the development of these mechanisms and their interactions in recent years.
心房颤动（AF）的发生是一个高度复杂的、多因素的过程，涉及病理生理机制、分子途径机制和许多遗传异常。病理生理机制包括离子通道改变、自主神经系统异常、炎症和 Ca2+处理异常。分子途径机制包括但不限于肾素-血管紧张素-醛固酮（RAAS）、转化生长因子-β（TGF-β）、氧化应激（OS）。尽管在临床实践中，AF 类型的区分，如阵发性和持续性，决定了治疗选择。然而，真正决定 AF 治疗效果和预后的是 AF 中存在的病理生理改变，而更重要的是其背后的分子机制和遗传改变。一个小小的线索揭示了总体趋势，小小的开端显示了事情的发展方向。本文将整理近年来这些机制及其相互作用的发展。
