心脏传导系统再生可预防心肌梗死后的心律失常。

IF 9.4 Q1 CARDIAC & CARDIOVASCULAR SYSTEMS Nature cardiovascular research Pub Date : 2025-01-03 DOI:10.1038/s44161-024-00586-x
Judy R Sayers, Hector Martinez-Navarro, Xin Sun, Carla de Villiers, Sarah Sigal, Michael Weinberger, Claudio Cortes Rodriguez, Leto Luana Riebel, Lucas Arantes Berg, Julia Camps, Neil Herring, Blanca Rodriguez, Tatjana Sauka-Spengler, Paul R Riley
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引用次数: 0

摘要

心律失常是心肌梗死(MI)的标志,并增加患者死亡率。心肌梗死后,对心脏传导系统的损伤是如何引起心律失常的尚不清楚。在这里,我们证明了新生小鼠心脏再生过程中的传导系统恢复与非再生阶段的病理重塑。组织清除的全器官成像发现心肌梗死和全身his -浦肯野损伤后传导纤维的无序束。单细胞RNA测序(scRNA-seq)揭示了在纤维化修复过程中再生传导网络与异常电改变的特定分子变化。这在功能上表现为从正常节律过渡到超出再生窗口的病理性传导延迟。正如在患者中观察到的那样,在梗死的人类心脏中建模暗示了非再生表型是导致心脏传导阻滞的原因。这些发现阐明了传导系统再生的机制,揭示了心肌梗死引起的损伤是如何引起临床心律失常的。
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Cardiac conduction system regeneration prevents arrhythmias after myocardial infarction.

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.

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