Sinus node dysfunction and atrial fibrillation—Relationships, clinical phenotypes, new mechanisms, and treatment approaches

Duan, Suhang; Du, Jianlin

doi:10.1016/j.arr.2023.101890

Cited by 6 publications

(3 citation statements)

References 179 publications

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“…In the heart, gap junctions offer pathways for intercellular current flow, thereby facilitating coordinated action potential propagation. Based on existing research, it appears that abnormalities in the gap junction may contribute to the development and maintenance of different types of cardiac arrhythmias [ 76 , 77 ]. It is evident that the toxicity of BPA in cardiovascular disease is compounded by the close cross-talk of various signaling pathways.…”

Section: Discussionmentioning

confidence: 99%

Exploring the mechanisms underlying effects of bisphenol a on cardiovascular disease by network toxicology and molecular docking

Xie,

Huang,

Zhao

et al. 2024

Heliyon

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Section: Discussionmentioning

confidence: 99%

Exploring the mechanisms underlying effects of bisphenol a on cardiovascular disease by network toxicology and molecular docking

Xie,

Huang,

Zhao

et al. 2024

Heliyon

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“…ДСУ чаще всего связана с возрастным прогрессирующим дегенеративным фиброзом ткани синусового узла (СУ) и окружающего предсердного миокарда [3][4][5]. Это может привести к патологии формирования и распространения импульса и может быть связано с различными синдромами брадикардии или паузами.…”

Section: ключевые моменты Key Messagesunclassified

Obstructive sleep apnea in bradyarrhythmias

Bulavina,

Vaisman,

Baimukanov

et al. 2024

Russ J Cardiol

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In recent decades, there has been increased interest in obstructive sleep apnea (OSA), especially in patients with a combination of OSA and sleep bradyarrhythmias. Worldwide, the diagnosis of OSA is steadily increasing. Increasingly, clinicians have begun to use CPAP therapy to treat sleep-related bradyarrhythmias. But in world practice there are no unambiguous guidelines for the management of this group of patients.

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“…Currently, 31 disease-causing variants in the KCNJ5 gene are known to date. Potential heart disease variants in KCNJ5 have been described and may be causative for long QT syndrome, Andersen-Tawil syndrome, atrial fibrillation, short QT syndrome, or unspecified events like sudden cardiac arrest or sudden unexpected death [21][22][23][24][25][26][27][28][29]. However, due to the small number of cases and mostly missing functional data, KCNJ5 is not a proven gene for the respective diseases.…”

Section: Introductionmentioning

confidence: 99%

The W101C KCNJ5 Mutation Induces Slower Pacing by Constitutively Active GIRK Channels in hiPSC-Derived Cardiomyocytes

Kayser,

Dittmann,

Šarić

et al. 2023

IJMS

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Mutations in the KCNJ5 gene, encoding one of the major subunits of cardiac G-protein-gated inwardly rectifying K+ (GIRK) channels, have been recently linked to inherited forms of sinus node dysfunction. Here, the pathogenic mechanism of the W101C KCNJ5 mutation underlying sinus bradycardia in a patient-derived cellular disease model of sinus node dysfunction (SND) was investigated. A human-induced pluripotent stem cell (hiPSCs) line of a mutation carrier was generated, and CRISPR/Cas9-based gene targeting was used to correct the familial mutation as a control line. Both cell lines were further differentiated into cardiomyocytes (hiPSC-CMs) that robustly expressed GIRK channels which underly the acetylcholine-regulated K+ current (IK,ACh). hiPSC-CMs with the W101C KCNJ5 mutation (hiPSCW101C-CM) had a constitutively active IK,ACh under baseline conditions; the application of carbachol was able to increase IK,ACh, further indicating that not all available cardiac GIRK channels were open at baseline. Additionally, hiPSCW101C-CM had a more negative maximal diastolic potential (MDP) and a slower pacing frequency confirming the bradycardic phenotype. Of note, the blockade of the constitutively active GIRK channel with XAF-1407 rescued the phenotype. These results provide further mechanistic insights and may pave the way for the treatment of SND patients with GIRK channel dysfunction.

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Sinus node dysfunction and atrial fibrillation—Relationships, clinical phenotypes, new mechanisms, and treatment approaches

Cited by 6 publications

References 179 publications

Exploring the mechanisms underlying effects of bisphenol a on cardiovascular disease by network toxicology and molecular docking

Exploring the mechanisms underlying effects of bisphenol a on cardiovascular disease by network toxicology and molecular docking

Obstructive sleep apnea in bradyarrhythmias

The W101C KCNJ5 Mutation Induces Slower Pacing by Constitutively Active GIRK Channels in hiPSC-Derived Cardiomyocytes

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