Abstract
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.
Highlights
Atrial fibrillation is characterized by chaotic, ectopic electrical activity and uncoordinated contraction [1]
There are complex and interesting electrical, structural and chemical interactions [9,10,11,12] between cardiac fibroblasts and myofibroblasts (collectively:fibroblasts) and myocytes, which are strongly affected by pathophysiological changes which give rise to inflammation, ischemia, fibrosis and altered morphology [11]
Interactions among myocytes,fibroblasts and epicardial adipose tissue will be explored, studying how the physical, chemical and electrotonic interplay may lead to fibrosis and both trigger and perpetuate atrial fibrillation
Summary
Atrial fibrillation is characterized by chaotic, ectopic electrical activity and uncoordinated contraction [1]. There are complex and interesting electrical, structural and chemical interactions [9,10,11,12] between cardiac fibroblasts and myofibroblasts (collectively: (myo)fibroblasts) and myocytes, which are strongly affected by pathophysiological changes which give rise to inflammation, ischemia, fibrosis and altered morphology [11]. These interactions may be instrumental in atrial remodeling which generates a substrate for fibrillation. Interactions among myocytes, (myo)fibroblasts and epicardial adipose tissue will be explored, studying how the physical, chemical and electrotonic interplay may lead to fibrosis and both trigger and perpetuate atrial fibrillation
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