About this Research Topic
In the last twenty years, the genetic basis of cardiac electrical phenotypes has been under deep investigation by many researchers worldwide. Recent results suggested that cardiac electrical related diseases, such as ventricular and atrial arrhythmias, were complex traits, influenced by a combination of genetic and environmental risk factors that contribute cumulatively to disease predisposition. It is clear that epigenetic modifications such as DNA methylation, histone modifications, and non-coding RNA-based mechanisms are the molecular targets for disadvantageous environmental stimuli and may lead to the onset and development of arrhythmia. However, understanding the functional impact of the epigenetic and transcriptional network in arrhythmias is still a major challenge. Further studies need to be done to clarify the molecular bases of the epigenetic and transcriptional network underlying various ventricular and atrial arrhythmias, so to provide a better understanding of the pathophysiology of cardiac electrical diseases.
This Research Topic provides us with an opportunity to deeply discuss the genetic and environmental factors as well as their interactions in cardiac electrical disease development. Cardiac electrical diseases, such as ventricular and atrial arrhythmias, were complex and heterogeneous diseases caused by different types of disturbances including structure and electrical remodeling. Although the role of epigenetic and transcriptional mechanisms in cardiovascular diseases has been under intense study during these years, its role in arrhythmias is still not clear. Therefore, it is necessary to clarify how epigenetic and transcriptional mechanisms impact the onset and development of arrhythmias and further identify new drug-gable targets in arrhythmia therapy.
We welcome submissions of focusing on, but not limited to, the following aspects:
1) Potential mechanisms linking epigenetics and ventricular and atrial arrhythmias (DNA methylation, Histone modification, Chromatin remodeling, et al).
2) Functional role of noncoding RNAs interaction and noncoding RNA-related regulatory pathways in ventricular and atrial arrhythmias.
3) Characteristics of gene and transcriptional regulatory network in different types of arrhythmias.
4) Epigenetic factors which can be developed as therapeutic targets for ventricular and atrial arrhythmias.
This Research Topic provides us with an opportunity to deeply discuss the genetic and environmental factors as well as their interactions in cardiac electrical disease development. Cardiac electrical diseases, such as ventricular and atrial arrhythmias, were complex and heterogeneous diseases caused by different types of disturbances including structure and electrical remodeling. Although the role of epigenetic and transcriptional mechanisms in cardiovascular diseases has been under intense study during these years, its role in arrhythmias is still not clear. Therefore, it is necessary to clarify how epigenetic and transcriptional mechanisms impact the onset and development of arrhythmias and further identify new drug-gable targets in arrhythmia therapy.
We welcome submissions of focusing on, but not limited to, the following aspects:
1) Potential mechanisms linking epigenetics and ventricular and atrial arrhythmias (DNA methylation, Histone modification, Chromatin remodeling, et al).
2) Functional role of noncoding RNAs interaction and noncoding RNA-related regulatory pathways in ventricular and atrial arrhythmias.
3) Characteristics of gene and transcriptional regulatory network in different types of arrhythmias.
4) Epigenetic factors which can be developed as therapeutic targets for ventricular and atrial arrhythmias.
Keywords: Epigenetics, Transcriptional regulation, Ventricular arrhythmias, Atrial arrhythmias, Regulatory network
Important Note: All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.
