Atrial fibrillation (AF) is the most common type of cardiac arrhythmia and is associated with high mortality and morbidity, thus representing a heavy socioeconomic burden worldwide. During atrial fibrillation, cardiac tissue undergoes multiple layers of remodeling from genetic to tissue level. All these processes promote atrial arrhythmias through active interactions between a set of electrophysiological, structural, inflammatory and genetic/regulatory factors. While fibrosis, myocyte hypertrophy and/or adiposity represent the hallmarks of structural remodeling of the atria, the intracellular Ca2+ handling abnormalities, as well as ion channels dysfunction, have been highlighted as important electrophysiological profibrillatory factors. These forms of remodeling can lead to triggered activity and electrical re-entry, which are major mechanisms of AF onset and progress. The importance of transcription factors and non-coding RNAs as regulators of gene expression has emerged in both electrical and structural remodelling related to atrial fibrillation.
Atrial fibrillation (AF) is the most prevalent cardiac arrhythmia in clinic. Atrial fibrillation is characterised by molecular, structural and electrical remodelling, including ion channel dysfunction, Ca2+-handling disturbances, and cardiomyocyte structural reshaping, which all together lead to severe complications such as stroke, heart failure (HF), and sudden death (SD). The substantial morbidity and mortality associated with the disease increase its management burden and the need for a better understanding of its underlying fundamental mechanisms, as well as for a more reliable therapeutic treatment. Although the past two decades witnessed significant advances in atrial fibrillation diagnosis and management, the gaps are still huge and the pathophysiological mechanisms behind atrial fibrillation onset and progress are still poorly understood. Therefore, mobilizing knowledge to improve our understanding of the atrial electrical, ionic/molecular and structural mechanisms that promote atrial fibrillation in the affected patients could help identifying new therapeutic targets/tools and then improve the patient’s quality of life.
This Research Topic will focus on the electrical, structural and molecular remodelling processes underlying atrial fibrillation initiation and maintenance and seeks to compile a series of high-quality research articles and up to date comprehensive reviews unveiling all aspects of atrial fibrillation mechanisms. Potential contribution topics include, but are not limited to:
- Cardiomyocyte remodelling
- Fibrosis
- Inflammation
- Arrhythmia
- Intracellular Ca2+ handling
- Ion channels dysfunction
- Transcription factors
- Non-coding-RNAs mediated gene regulation
Contributions on other significant topics that provide knowledge that might open the way to new therapeutic tools for atrial fibrillation are also welcome.
Atrial fibrillation (AF) is the most common type of cardiac arrhythmia and is associated with high mortality and morbidity, thus representing a heavy socioeconomic burden worldwide. During atrial fibrillation, cardiac tissue undergoes multiple layers of remodeling from genetic to tissue level. All these processes promote atrial arrhythmias through active interactions between a set of electrophysiological, structural, inflammatory and genetic/regulatory factors. While fibrosis, myocyte hypertrophy and/or adiposity represent the hallmarks of structural remodeling of the atria, the intracellular Ca2+ handling abnormalities, as well as ion channels dysfunction, have been highlighted as important electrophysiological profibrillatory factors. These forms of remodeling can lead to triggered activity and electrical re-entry, which are major mechanisms of AF onset and progress. The importance of transcription factors and non-coding RNAs as regulators of gene expression has emerged in both electrical and structural remodelling related to atrial fibrillation.
Atrial fibrillation (AF) is the most prevalent cardiac arrhythmia in clinic. Atrial fibrillation is characterised by molecular, structural and electrical remodelling, including ion channel dysfunction, Ca2+-handling disturbances, and cardiomyocyte structural reshaping, which all together lead to severe complications such as stroke, heart failure (HF), and sudden death (SD). The substantial morbidity and mortality associated with the disease increase its management burden and the need for a better understanding of its underlying fundamental mechanisms, as well as for a more reliable therapeutic treatment. Although the past two decades witnessed significant advances in atrial fibrillation diagnosis and management, the gaps are still huge and the pathophysiological mechanisms behind atrial fibrillation onset and progress are still poorly understood. Therefore, mobilizing knowledge to improve our understanding of the atrial electrical, ionic/molecular and structural mechanisms that promote atrial fibrillation in the affected patients could help identifying new therapeutic targets/tools and then improve the patient’s quality of life.
This Research Topic will focus on the electrical, structural and molecular remodelling processes underlying atrial fibrillation initiation and maintenance and seeks to compile a series of high-quality research articles and up to date comprehensive reviews unveiling all aspects of atrial fibrillation mechanisms. Potential contribution topics include, but are not limited to:
- Cardiomyocyte remodelling
- Fibrosis
- Inflammation
- Arrhythmia
- Intracellular Ca2+ handling
- Ion channels dysfunction
- Transcription factors
- Non-coding-RNAs mediated gene regulation
Contributions on other significant topics that provide knowledge that might open the way to new therapeutic tools for atrial fibrillation are also welcome.
