Sayers Judy R, Martinez-Navarro Hector, Sun Xin, de Villiers Carla, Sigal Sarah, Weinberger Michael, Rodriguez Claudio Cortes, Riebel Leto Luana, Berg Lucas Arantes, Camps Julia, Herring Neil, Rodriguez Blanca, Sauka-Spengler Tatjana, Riley Paul R
Institute of Developmental and Regenerative Medicine, University of Oxford, Oxford, UK.
Department of Physiology, Anatomy and Genetics, University of Oxford, Oxford, UK.
Nat Cardiovasc Res. 2025 Feb;4(2):163-179. doi: 10.1038/s44161-024-00586-x. Epub 2025 Jan 3.
Arrhythmias are a hallmark of myocardial infarction (MI) and increase patient mortality. How insult to the cardiac conduction system causes arrhythmias following MI is poorly understood. Here, we demonstrate conduction system restoration during neonatal mouse heart regeneration versus pathological remodeling at non-regenerative stages. Tissue-cleared whole-organ imaging identified disorganized bundling of conduction fibers after MI and global His-Purkinje disruption. Single-cell RNA sequencing (scRNA-seq) revealed specific molecular changes to regenerate the conduction network versus aberrant electrical alterations during fibrotic repair. This manifested functionally as a transition from normal rhythm to pathological conduction delay beyond the regenerative window. Modeling in the infarcted human heart implicated the non-regenerative phenotype as causative for heart block, as observed in patients. These findings elucidate the mechanisms underpinning conduction system regeneration and reveal how MI-induced damage elicits clinical arrhythmogenesis.
心律失常是心肌梗死(MI)的一个标志,会增加患者死亡率。心肌梗死后,心脏传导系统受到损伤如何导致心律失常,目前还知之甚少。在这里,我们展示了新生小鼠心脏再生过程中的传导系统恢复,以及非再生阶段的病理重塑。组织透明化的全器官成像显示,心肌梗死后传导纤维束紊乱,希氏-浦肯野系统整体破坏。单细胞RNA测序(scRNA-seq)揭示了再生传导网络时的特定分子变化,以及纤维化修复过程中的异常电改变。这在功能上表现为从正常节律转变为再生窗口之后的病理性传导延迟。在梗死的人类心脏中进行的建模表明,正如在患者身上观察到的那样,非再生表型是心脏传导阻滞的病因。这些发现阐明了传导系统再生的机制,并揭示了心肌梗死引起的损伤如何引发临床心律失常。