找到用于预防心律失常的兰尼碱受体2（RyR2）磷酸化的合适平衡点。 - Suppr

Finding the right balance of RyR2 phosphorylation for arrhythmia prevention.

作者信息

Blackwell Daniel J, Knollmann Björn C

机构信息

Vanderbilt Center for Arrhythmia Research and Therapeutics, Department of Medicine, Vanderbilt University Medical Center, Nashville, TN, USA.

出版信息

Nat Cardiovasc Res. 2025 Aug;4(8):962-963. doi: 10.1038/s44161-025-00701-6.

DOI:10.1038/s44161-025-00701-6

PMID:40797045

Abstract

摘要

相似文献

Finding the right balance of RyR2 phosphorylation for arrhythmia prevention.找到用于预防心律失常的兰尼碱受体2（RyR2）磷酸化的合适平衡点。

Nat Cardiovasc Res. 2025 Aug;4(8):962-963. doi: 10.1038/s44161-025-00701-6.

Ablation of three major phospho-sites in RyR2 preserves the global adrenergic response but creates an arrhythmogenic substrate.去除兰尼碱受体2（RyR2）中的三个主要磷酸化位点可保留整体肾上腺素能反应，但会产生致心律失常底物。

bioRxiv. 2024 Jul 9:2024.07.08.602617. doi: 10.1101/2024.07.08.602617.

Preventing the phosphorylation of RyR2 at canonical sites reduces Ca leak and promotes arrhythmia by reactivating the I current.阻止兰尼碱受体2（RyR2）在典型位点的磷酸化可减少钙泄漏，并通过重新激活I电流促进心律失常。

Nat Cardiovasc Res. 2025 Aug;4(8):976-990. doi: 10.1038/s44161-025-00693-3. Epub 2025 Aug 12.

Structural instability of ryanodine receptor 2 causes endoplasmic reticulum (ER) dysfunction as well as sarcoplasmic reticulum (SR) dysfunction.兰尼碱受体2的结构不稳定性会导致内质网（ER）功能障碍以及肌浆网（SR）功能障碍。

J Cardiol. 2025 Feb 8. doi: 10.1016/j.jjcc.2025.02.003.

Phosphorylation of RyR2 simultaneously expands the dyad and rearranges the tetramers.RyR2 的磷酸化同时扩张了二联体并重新排列了四聚体。

J Gen Physiol. 2024 Apr 1;156(4). doi: 10.1085/jgp.202213108. Epub 2024 Feb 22.

Microgravity-Induced Cognitive Decline: Investigating the Pathogenic Mechanisms of RyR2 Hyperphosphorylation and S107 Intervention.

FASEB J. 2025 Jul 15;39(13):e70743. doi: 10.1096/fj.202500756RR.

Quantification of Sarcoplasmic Reticulum Ca Release in Primary Ventricular Cardiomyocytes.定量分析原发性心室心肌细胞肌浆网钙释放。

Curr Protoc. 2024 Nov;4(11):e70048. doi: 10.1002/cpz1.70048.

Wnt/β-catenin pathway induces cardiac dysfunction via AKAP6-mediated RyR2 phosphorylation and sarcoplasmic reticulum calcium leakage.Wnt/β-连环蛋白信号通路通过AKAP6介导的兰尼碱受体2磷酸化和肌浆网钙泄漏诱导心脏功能障碍。

J Mol Cell Biol. 2025 Jul 28;17(2). doi: 10.1093/jmcb/mjaf002.

Pharmacological study of the safety, efficacy, and potential of M201-A on paroxysmal and persistent atrial fibrillation.M201-A对阵发性和持续性心房颤动的安全性、疗效及潜力的药理学研究

J Pharmacol Exp Ther. 2025 Aug;392(8):103652. doi: 10.1016/j.jpet.2025.103652. Epub 2025 Jul 2.

Structure-activity optimization of ryanodine receptor modulators for the treatment of catecholaminergic polymorphic ventricular tachycardia.用于治疗儿茶酚胺能多形性室性心动过速的雷诺丁受体调节剂的构效优化

Heart Rhythm. 2024 Oct 2. doi: 10.1016/j.hrthm.2024.09.062.

本文引用的文献

The drug-elicitable alternative splicing module for tunable vector expression in the heart.用于心脏中可调载体表达的药物诱导性可变剪接模块。

Nat Cardiovasc Res. 2025 Jun 13. doi: 10.1038/s44161-025-00665-7.

Inhibitors of Intracellular RyR2 Calcium Release Channels as Therapeutic Agents in Arrhythmogenic Heart Diseases.细胞内兰尼碱受体2型钙释放通道抑制剂作为致心律失常性心脏病的治疗药物

Annu Rev Pharmacol Toxicol. 2025 Jan;65(1):443-463. doi: 10.1146/annurev-pharmtox-061724-080739. Epub 2024 Dec 17.

Dual ablation of the RyR2-Ser2808 and RyR2-Ser2814 sites increases propensity for pro-arrhythmic spontaneous Ca releases.双重消融 RyR2-Ser2808 和 RyR2-Ser2814 位点可增加致心律失常性自发性 Ca 释放的倾向。

J Physiol. 2024 Oct;602(20):5179-5201. doi: 10.1113/JP286453. Epub 2024 Sep 24.

Cardiac ryanodine receptor calcium release deficiency syndrome.心脏兰尼碱受体钙释放缺陷综合征。

Sci Transl Med. 2021 Feb 3;13(579). doi: 10.1126/scitranslmed.aba7287.

Loss of SPEG Inhibitory Phosphorylation of Ryanodine Receptor Type-2 Promotes Atrial Fibrillation.肌联蛋白受体型 2 的 SPEG 抑制性磷酸化丧失促进心房颤动。

Circulation. 2020 Sep 22;142(12):1159-1172. doi: 10.1161/CIRCULATIONAHA.120.045791. Epub 2020 Jul 20.

Phosphorylation of the ryanodine receptor 2 at serine 2030 is required for a complete β-adrenergic response.ryanodine 受体 2 丝氨酸 2030 位点的磷酸化是完全β-肾上腺素能反应所必需的。

J Gen Physiol. 2019 Feb 4;151(2):131-145. doi: 10.1085/jgp.201812155. Epub 2018 Dec 12.

A Single Protein Kinase A or Calmodulin Kinase II Site Does Not Control the Cardiac Pacemaker Ca2+ Clock.单一的蛋白激酶A或钙调蛋白激酶II位点并不控制心脏起搏器Ca2+时钟。

Circ Arrhythm Electrophysiol. 2016 Feb;9(2):e003180. doi: 10.1161/CIRCEP.115.003180.

Delayed afterdepolarizations generate both triggers and a vulnerable substrate promoting reentry in cardiac tissue.延迟后除极既产生触发因素，又形成一个易损基质，促进心脏组织中的折返。

Heart Rhythm. 2015 Oct;12(10):2115-24. doi: 10.1016/j.hrthm.2015.06.019. Epub 2015 Jun 10.

Role of RyR2 phosphorylation in heart failure and arrhythmias: protein kinase A-mediated hyperphosphorylation of the ryanodine receptor at serine 2808 does not alter cardiac contractility or cause heart failure and arrhythmias.兰尼碱受体2（RyR2）磷酸化在心力衰竭和心律失常中的作用：蛋白激酶A介导的兰尼碱受体在丝氨酸2808处的过度磷酸化不会改变心脏收缩力，也不会导致心力衰竭和心律失常。

Circ Res. 2014 Apr 11;114(8):1320-7; discussion 1327. doi: 10.1161/CIRCRESAHA.114.300569.

Role of RyR2 phosphorylation in heart failure and arrhythmias: Controversies around ryanodine receptor phosphorylation in cardiac disease.兰尼碱受体2磷酸化在心力衰竭和心律失常中的作用：心脏病中围绕兰尼碱受体磷酸化的争议

Circ Res. 2014 Apr 11;114(8):1311-9; discussion 1319. doi: 10.1161/CIRCRESAHA.114.300568.

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Finding the right balance of RyR2 phosphorylation for arrhythmia prevention.

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