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Emerging Signaling Regulation of Sinoatrial Node Dysfunction

  • Regenerative Medicine (SM Wu, Section Editor)
  • Published:
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Abstract

Purpose of Review

The sinoatrial node (SAN), the natural pacemaker of the heart, is responsible for generating electrical impulses and initiating each heartbeat. Sinoatrial node dysfunction (SND) causes various arrhythmias such as sinus arrest, SAN block, and tachycardia/bradycardia syndrome. Unraveling the underlying mechanisms of SND is of paramount importance in the pursuit of developing effective therapeutic strategies for patients with SND. This review provides a concise summary of the most recent progress in the signaling regulation of SND.

Recent Findings

Recent studies indicate that SND can be caused by abnormal intercellular and intracellular signaling, various forms of heart failure (HF), and diabetes. These discoveries provide novel insights into the underlying mechanisms SND, advancing our understanding of its pathogenesis.

Summary

SND can cause severe cardiac arrhythmias associated with syncope and an increased risk of sudden death. In addition to ion channels, the SAN is susceptible to the influence of various signalings including Hippo, AMP-activated protein kinase (AMPK), mechanical force, and natriuretic peptide receptors. New cellular and molecular mechanisms related to SND are also deciphered in systemic diseases such as HF and diabetes. Progress in these studies contributes to the development of potential therapeutics for SND.

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Funding

M.Z. is supported by the funding provided by the American Heart Association (902940). J.W. is supported by the funding provided by the National Institutes of Health (R01HL142704) and the American Heart Association (970606 and 23EIA1039128).

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M.Z. and Y.C wrote the original draft. M.Z., Y.C, S.E., and J.W. reviewed and edited the manuscript. All authors have read and agreed to the published version of the manuscript.

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Correspondence to Jun Wang.

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Zheng, M., Erhardt, S., Cao, Y. et al. Emerging Signaling Regulation of Sinoatrial Node Dysfunction. Curr Cardiol Rep 25, 621–630 (2023). https://doi.org/10.1007/s11886-023-01885-8

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