Genetics and Epigenetics of Atrial Fibrillation

Lozano-Velasco, Estefanía; Franco, Diego; Aránega, Amelia; Daimi, Houria

doi:10.3390/ijms21165717

Cited by 64 publications

(53 citation statements)

References 232 publications

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“…This topic, however, lies beyond the scope of this review and is well reviewed elsewhere 57–60 . Since the first discovered mutation related to AF, S140G, advancements in genetic (mutations related to ion channels, cardiogenesis, and fibrosis) and epigenetic (microRNAs, long non‐coding RNAs) modifications have shed light on the relationship between DNA and AF 23 . Below, we highlight some basic novel findings regarding the main substrates responsible for AF initiation and perpetuation (Figure 1).…”

Section: Pathophysiological Mechanisms Of Af Related To Eatmentioning

confidence: 99%

“…Age, 12,13 hypertension, 14,15 diabetes mellitus (DM), 16,17 and obstructive sleep apnea 18 are well‐known risk factors for AF 19 . In addition, smoking, 20 alcohol consumption, 21 lifestyle, 22 and genetic predisposition 23,24 have been recognized as important players in the susceptibility, maintenance, and recurrence of AF. This review is focused on obesity, more specifically, on epicardial fat and its role in AF.…”

Section: Af: Prevalence Incidence Classification and Etiologymentioning

confidence: 99%

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Updates on epicardial adipose tissue mechanisms on atrial fibrillation

et al. 2021

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Summary Obesity is a well‐known risk factor for atrial fibrillation (AF). Local epi‐myocardial or intra‐myocardial adiposity caused by aging, obesity, or cardiovascular disease (CVD) is considered to be a better predictor of the risk of AF than general adiposity. Some of the described mechanisms suggest that epicardial adipose tissue (EAT) participates in structural remodeling owing to its endocrine activity or its infiltration between cardiomyocytes. Epicardial fat also wraps up the ganglionated plexi that reach the myocardium. Although the increment of volume/thickness and activity of EAT might modify autonomic activity, autonomic system dysfunction might also change the endocrine activity of epicardial fat in a feedback response. As a result, new preventive therapeutic strategies are focused on reducing adiposity and weight loss before AF ablation or inhibiting autonomic neurotransmitter secretion on fat pads during open‐heart surgery to reduce the recurrence or postoperative risk of AF. In this manuscript, we review some of the novel findings regarding the pathophysiology and associated risk factors of AF, with special emphasis on the role of EAT in the electrical, structural, and molecular mechanisms of AF initiation and maintenance. In addition, we have included a brief note provided on epicardial fat preclinical models that could be useful for identifying new therapeutic targets.

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Section: Pathophysiological Mechanisms Of Af Related To Eatmentioning

confidence: 99%

Section: Af: Prevalence Incidence Classification and Etiologymentioning

confidence: 99%

Updates on epicardial adipose tissue mechanisms on atrial fibrillation

et al. 2021

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“…These candidate genes have been identified mostly through genome wide association studies (GWAS) and familial studies demonstrating that atrial fibrillation can be inherited [ 116 , 120 , 121 ]. Many of these genes identified have been linked to genes that code for ion channels, or are involved in fibrosis nuclear structure, cardiogenesis, extracellular matrix remodeling and cell–cell coupling [ 122 ]. The genetics of atrial fibrillation can provide new insights into disease processes and novel therapeutic targets, however, recent research is also exploring the role epigenetics plays in the pathophysiology of atrial fibrillation.…”

Section: Conclusion Challenges and Future Directionsmentioning

confidence: 99%

Are Interactions between Epicardial Adipose Tissue, Cardiac Fibroblasts and Cardiac Myocytes Instrumental in Atrial Fibrosis and Atrial Fibrillation?

Krishnan

Chilton

Raman

et al. 2021

Cells

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Atrial fibrillation is very common among the elderly and/or obese. While myocardial fibrosis is associated with atrial fibrillation, the exact mechanisms within atrial myocytes and surrounding non-myocytes are not fully understood. This review considers the potential roles of myocardial fibroblasts and myofibroblasts in fibrosis and modulating myocyte electrophysiology through electrotonic interactions. Coupling with (myo)fibroblasts in vitro and in silico prolonged myocyte action potential duration and caused resting depolarization; an optogenetic study has verified in vivo that fibroblasts depolarized when coupled myocytes produced action potentials. This review also introduces another non-myocyte which may modulate both myocardial (myo)fibroblasts and myocytes: epicardial adipose tissue. Epicardial adipocytes are in intimate contact with myocytes and (myo)fibroblasts and may infiltrate the myocardium. Adipocytes secrete numerous adipokines which modulate (myo)fibroblast and myocyte physiology. These adipokines are protective in healthy hearts, preventing inflammation and fibrosis. However, adipokines secreted from adipocytes may switch to pro-inflammatory and pro-fibrotic, associated with reactive oxygen species generation. Pro-fibrotic adipokines stimulate myofibroblast differentiation, causing pronounced fibrosis in the epicardial adipose tissue and the myocardium. Adipose tissue also influences myocyte electrophysiology, via the adipokines and/or through electrotonic interactions. Deeper understanding of the interactions between myocytes and non-myocytes is important to understand and manage atrial fibrillation.

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“…Genome-wide association studies (GWAS) have uncovered over 100 AF associated genetic loci (5). But none has been identified to be a potential therapeutic target, indicating additional candidates to AF pathophysiology.…”

Section: Introductionmentioning

confidence: 99%

Epigenetic Mechanism and Therapeutic Implications of Atrial Fibrillation

Nie²,

Han³

et al. 2022

Front. Cardiovasc. Med.

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Atrial fibrillation (AF) is the most common arrhythmia attacking 1. 5–2.0% of general population worldwide. It has a significant impact on morbidity and mortality globally and its prevalence increases exponentially with age. Therapies like catheter ablation or conventional antiarrhythmic drugs have not provided effective solution to the recurrence for AF over the past decades. Over 100 genetic loci have been discovered to be associated with AF by Genome-wide association studies (GWAS) but none has led to a therapy. Recently potential involvement of epigenetics (DNA methylation, histone modification, and non-coding RNAs) in the initiation and maintenance of AF has partly emerged as proof-of-concept in the mechanism and management of AF. Here we reviewed the epigenetic features involved in AF pathophysiology and provided an update of their implications in AF therapy.

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Genetics and Epigenetics of Atrial Fibrillation

Cited by 64 publications

References 232 publications

Updates on epicardial adipose tissue mechanisms on atrial fibrillation

Updates on epicardial adipose tissue mechanisms on atrial fibrillation

Are Interactions between Epicardial Adipose Tissue, Cardiac Fibroblasts and Cardiac Myocytes Instrumental in Atrial Fibrosis and Atrial Fibrillation?

Epigenetic Mechanism and Therapeutic Implications of Atrial Fibrillation

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