KCNN3 SNP rs13376333 on Chromosome 1q21 Confers Increased Risk of Atrial Fibrillation

Yao, Jialu; Zhou, Yafeng; Yang, Xiangjun; Qian, Xiaodong; Jiang, Wenping

doi:10.1536/ihj.15-133

Cited by 12 publications

(4 citation statements)

References 28 publications

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“…[30] ZFHX3 knockdown in atrial myocytes dysregulated calcium homeostasis and increased atrial arrhythmogenesis, ultimately contributing to AF occurrence. [31] Studies found rs13376333, rs7193343, and rs2106261 increased risk of AF [32–34] and some studies also involved in their relationship on AF recurrence. [3,4,23,35] Therefore, we also pooled the HRs of rs13376333, rs7193343, and rs2106261 variants on AF recurrence.…”

Section: Discussionmentioning

confidence: 99%

Association between gene variants and the recurrence of atrial fibrillation

Jiang¹,

Wang²,

Qu³

et al. 2019

Medicine

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Background: Studies showed the controversial results about the effect of common genetic polymorphisms on the atrial fibrillation (AF) recurrence. We performed the systematic review and meta-analysis to qualify the association between common genetic polymorphisms and AF recurrence. Methods: Articles were systematically retrieved PubMed, Web of Science, EMBASE, Wanfang, and CNKI database and 9 studies including 3204 patients were enrolled in our meta-analysis. Results: Results showed that the associations were significant under rs2200733 3 genetic models (TT vs CC: odds ratio [OR] [confidence interval [CI]] = 1.336 [1.061–1.683], P = .014; CT vs CC: OR [CI] = 0.759 [0.614–0.937], P = .01; TT vs CT + CC: OR [CI] = 2.308 [1.440–3.700], P = .001). The association was significant under rs10033464 genetic model (TT vs GG: OR [CI] = 1.517 [1.165–1.976], P = .002). Conclusions: Rs13376333 on chromosome 1q21 (in KCNN3 ), rs7193343 and rs2106261 on chromosome 16q22 (in ZFHX3 ) were not associated with AF recurrence in our meta-analysis. In total, our meta-analysis found that rs2200733 and rs10033464 on chromosome 4q25 (near PITX2 ) were associated with the risk of AF recurrence.

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Section: Discussionmentioning

confidence: 99%

Association between gene variants and the recurrence of atrial fibrillation

Jiang¹,

Wang²,

Qu³

et al. 2019

Medicine

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“…22) Previous studies have documented that in some familial AF patients, novel susceptibility genes are responsible for electrical abnormalities leading to AF in the absence of structural remodeling. [23][24][25][26][27][28] These specific genes are related to the many channelopathies present in both the atria and ventricles via gain-of-function or loss-of-function of specific ion currents.…”

Section: Discussionmentioning

confidence: 99%

Incidence of Atrial Tachyarrhythmias in Patients With Early Repolarization Syndrome

et al. 2017

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SummaryAtrial tachyarrhythmias (ATAs) occur in a significant proportion of Brugada syndrome (BrS) patients and are often an important cause of inappropriate shocks. The aim of this retrospective study was to evaluate the incidence of ATAs and ATA-induced inappropriate shocks in early repolarization syndrome (ERS) patients as compared to BrS patients.We analyzed data from 20 consecutive patients who were diagnosed with ERS and compared them with patients diagnosed with BrS (n = 31). Clinical and ICD interrogation data were collected and analyzed for all events with ICD shocks.Three patients had a history of atrial fibrillation (AF) prior to ICD implantation. One patient had AV reentrant tachycardia and was successfully ablated before ICD implantation. ATAs were newly diagnosed in 4 patients with no prior history of AF. There were no significant differences in gender, age, or left atrial diameter between ATA development. Four (20%) of 20 consecutive patients received inappropriate ICD shocks for ATAs. One suffered from repeat inappropriate shocks triggered by paroxysmal AF and received catheter ablation for AF.ATAs were not infrequent in patients with ERS and seemed to be related to inappropriate ICD therapy. Careful ICD programming is required to reduce ATA-related inappropriate ICD shock in patients with ERS. (Int Heart J 2017; 58: 43-49) Key words: Early repolarization syndrome, Brugada syndrome, Sudden cardiac death E arly repolarization syndrome (ERS) has recently been uncovered as an important cause of sudden cardiac death (SCD) or life-threatening arrhythmias in patients with structurally normal hearts.1-3) Several basic studies reported that transmural or epicardial dispersion of action potentials in the early repolarization phase is responsible for the electrocardiographic phenotype of the ST segment and J wave elevation, suggesting a common electrophysiologic background between Brugada syndrome (BrS) and ERS. 4,5) A significant proportion of patients with BrS develop atrial tachyarrhythmias (ATAs), which are often an important cause of inappropriate shock. [6][7][8][9] There are many similarities between BrS and ERS in clinical and electrocardiographic characteristics.5) As the dysfunction of cardiac ion channels is not limited to the ventricular myocardium, it may be possible that electrical abnormalities coexist in the atrial and ventricular myocardium of patients with ERS. Gain or loss-of-function mutations in atrial ion channels may lead to shortening or prolongation of atrial action potential durations, resulting in increased dispersion of atrial repolarization or intra-atrial conduction time in patients with ERS. The aim of this retrospective study was to evaluate the incidence of ATAs and ATAinduced inappropriate shock in patients with ERS as compared to those with BrS.

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“…Interestingly, it has been reported by several studies that there are significant associations between the single nucleotide polymorphism rs13376333 in KCNN3 on chromosome 1q21 and the risk of developing AF in Chinese and European ancestry [36][37][38]. Moreover, atrial miRNA-499, an important regulator of KCNN3 gene expression, was upregulated by 2.33-fold in atria with AF, resulting in downregulation of SK3 protein expression by 46% [39].…”

Section: Figurementioning

confidence: 99%

Modulation of SK Channels: Insight Into Therapeutics of Atrial Fibrillation

Qian

Wang

2021

Heart, Lung and Circulation

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Atrial fibrillation (AF) is the most prevalent cardiac arrhythmia in the world. Although much technological progress in the treatment of AF has been made, there is an urgent need for better treatment of AF due to its high rates of morbidity and mortality. The anti-arrhythmic drugs currently approved for marketing have significant limitations and side effects such as life-threatening ventricular arrhythmias and hypotension. The small conductance Ca 21-activated K 1 channels (SK channels) are dependent on intracellular Ca 21 concentrations, which tightly integrate with membrane potential. Given the predominant expression in the atria of many species, including humans, they are now emerging as a therapeutic target for treating AF. This review aimed to illustrate the characteristics and function of SK channels. Moreover, it discussed the regulation of SK channels and their potential as a therapeutic target of AF.

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KCNN3 SNP rs13376333 on Chromosome 1q21 Confers Increased Risk of Atrial Fibrillation

Cited by 12 publications

References 28 publications

Association between gene variants and the recurrence of atrial fibrillation

Association between gene variants and the recurrence of atrial fibrillation

Incidence of Atrial Tachyarrhythmias in Patients With Early Repolarization Syndrome

Modulation of SK Channels: Insight Into Therapeutics of Atrial Fibrillation

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