Sleep apnea and atrial fibrillation: Update 2020

Linz, Dominik; Dobrev, Dobromir

doi:10.1016/j.ijcha.2020.100681

Cited by 3 publications

(3 citation statements)

References 42 publications

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“…Lin et al revealed that atrial fibrillation burden is a sex-specific risk factor for OSA and is limited to male. 45 Moreover, women with both AF and OSA have a lower AF burden than men, despite being older and having similar OSA severity and body habitus. 45 Thus, we think this could also result in the difference of these studies.…”

Section: Discussionmentioning

confidence: 99%

“…45 Moreover, women with both AF and OSA have a lower AF burden than men, despite being older and having similar OSA severity and body habitus. 45 Thus, we think this could also result in the difference of these studies. Besides, the experimental procedures and duration of CIH are also different between our study and the work by Castro-Grattoni.…”

Section: Discussionmentioning

confidence: 99%

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Berberine ameliorates chronic intermittent hypoxia‐induced cardiac remodelling by preserving mitochondrial function, role of SIRT6 signalling

Zhou,

Zhao,

Huang

et al. 2024

J Cellular Molecular Medi

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Chronic intermittent hypoxia (CIH) is associated with an increased risk of cardiovascular diseases. Previously, we have shown that berberine (BBR) is a potential cardioprotective agent. However, its effect and mechanism on CIH‐induced cardiomyopathy remain uncovered. This study was designed to determine the effects of BBR against CIH‐induced cardiac damage and to explore the molecular mechanisms. Mice were exposed to 5 weeks of CIH with or without the treatment of BBR and adeno‐associated virus 9 (AAV9) carrying SIRT6 or SIRT6‐specific short hairpin RNA. The effect of BBR was evaluated by echocardiography, histological analysis and western blot analysis. CIH caused the inactivation of myocardial SIRT6 and AMPK‐FOXO3a signalling. BBR dose‐dependently ameliorated cardiac injury in CIH‐induced mice, as evidenced by increased cardiac function and decreased fibrosis. Notably, SIRT6 overexpression mimicked these beneficial effects, whereas infection with recombinant AAV9 carrying SIRT6‐specific short hairpin RNA abrogated them. Mechanistically, BBR reduced oxidative stress damage and preserved mitochondrial function via activating SIRT6‐AMPK‐FOXO3a signalling, enhancing mitochondrial biogenesis as well as PINK1‐Parkin‐mediated mitophagy. Taken together, these data demonstrate that SIRT6 activation protects against the pathogenesis of CIH‐induced cardiac dysfunction. BBR attenuates CIH‐induced myocardial injury by improving mitochondrial biogenesis and PINK1‐Parkin‐dependent mitophagy via the SIRT6‐AMPK‐FOXO3a signalling pathway.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Berberine ameliorates chronic intermittent hypoxia‐induced cardiac remodelling by preserving mitochondrial function, role of SIRT6 signalling

Zhou,

Zhao,

Huang

et al. 2024

J Cellular Molecular Medi

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“…The evolution of the arrhythmogenic substrate due to atrial remodeling is promoted by cardiac and non-cardiac diseases, risk factors such as obesity and aging, and AF itself [12,[29][30][31]. Atrial electrical remodeling includes Ca 2+ -handling abnormalities and changes in ion current properties that promote re-entry by abbreviating APD and effective refractory period (ERP) [32,33].…”

Section: General Mechanisms Of Afmentioning

confidence: 99%

Emerging Antiarrhythmic Drugs for Atrial Fibrillation

Saljic

Heijman

Dobrev

2022

IJMS

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Atrial fibrillation (AF), the most common cardiac arrhythmia worldwide, is driven by complex mechanisms that differ between subgroups of patients. This complexity is apparent from the different forms in which AF presents itself (post-operative, paroxysmal and persistent), each with heterogeneous patterns and variable progression. Our current understanding of the mechanisms responsible for initiation, maintenance and progression of the different forms of AF has increased significantly in recent years. Nevertheless, antiarrhythmic drugs for the management of AF have not been developed based on the underlying arrhythmia mechanisms and none of the currently used drugs were specifically developed to target AF. With the increased knowledge on the mechanisms underlying different forms of AF, new opportunities for developing more effective and safer AF therapies are emerging. In this review, we provide an overview of potential novel antiarrhythmic approaches based on the underlying mechanisms of AF, focusing both on the development of novel antiarrhythmic agents and on the possibility of repurposing already marketed drugs. In addition, we discuss the opportunity of targeting some of the key players involved in the underlying AF mechanisms, such as ryanodine receptor type-2 (RyR2) channels and atrial-selective K+-currents (IK2P and ISK) for antiarrhythmic therapy. In addition, we highlight the opportunities for targeting components of inflammatory signaling (e.g., the NLRP3-inflammasome) and upstream mechanisms targeting fibroblast function to prevent structural remodeling and progression of AF. Finally, we critically appraise emerging antiarrhythmic drug principles and future directions for antiarrhythmic drug development, as well as their potential for improving AF management.

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