About this Research Topic
Arrhythmia comprises the abnormality or perturbation in the normal activation sequence within the heart while heart failure is a clinical syndrome featured by systemic perfusion inadequate to meet the body's metabolic demands, which is caused by impaired cardiac pump function. Besides happening separately, arrhythmia and heart failure often interact as both cause and effect. Overall, arrhythmia and heart failure have become a growing global epidemic and a financial burden for society. However, the current management strategies for arrhythmia and heart failure are relative suboptimal. A better understanding of the molecular mechanism of arrhythmia and heart failure will facilitate the process of the development of novel anti-arrhythmia and heart failure drugs.
In the past few years, researchers have unraveled some genetic and epigenetic basis of arrhythmia and heart failure. Take atrial fibrillation (AF), the most prevalent arrhythmia in the clinic, as an example, at least 2 chromosomal loci and 17 causal mutations have been identified in familial AF, and an additional 7 common variants and single-nucleotide polymorphisms in 11 different genes have been indicated in nonfamilial AF, indicating a genetic susceptibility to the development of AF. Recent insights into the genetic causes of myocardial diseases also highlighted the importance of single-gene defects in heart failure.
Unlike the genetic factors, epigenetic factors basically regulate gene expression through modification of chromosomal components without an alteration in the nucleotide sequence of the genome. However, it is already becoming evident that epigenetic factors such as microRNAs, also contribute to the genesis of AF. Moreover, recent genetic and biochemical analyses have also indicated that epigenetic changes play an important role in the development of heart failure.
Advances in understanding the genetics and epigenetic basis of arrhythmia and heart failure could provide the opportunity for facilitating the development of new genetic and/or epigenetics-based therapies. Never before has such an opportunity arisen to advance our understanding of the biology of arrhythmia and heart failure through the translation of genetics and epigenetics findings from the bench to the bedside.
In the past few years, researchers have unraveled some genetic and epigenetic basis of arrhythmia and heart failure. Take atrial fibrillation (AF), the most prevalent arrhythmia in the clinic, as an example, at least 2 chromosomal loci and 17 causal mutations have been identified in familial AF, and an additional 7 common variants and single-nucleotide polymorphisms in 11 different genes have been indicated in nonfamilial AF, indicating a genetic susceptibility to the development of AF. Recent insights into the genetic causes of myocardial diseases also highlighted the importance of single-gene defects in heart failure.
Unlike the genetic factors, epigenetic factors basically regulate gene expression through modification of chromosomal components without an alteration in the nucleotide sequence of the genome. However, it is already becoming evident that epigenetic factors such as microRNAs, also contribute to the genesis of AF. Moreover, recent genetic and biochemical analyses have also indicated that epigenetic changes play an important role in the development of heart failure.
Advances in understanding the genetics and epigenetic basis of arrhythmia and heart failure could provide the opportunity for facilitating the development of new genetic and/or epigenetics-based therapies. Never before has such an opportunity arisen to advance our understanding of the biology of arrhythmia and heart failure through the translation of genetics and epigenetics findings from the bench to the bedside.
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