Study of the role of cardiac fibroblasts underlying the transition of paroxysmal to persistent atrial fibrillation.

Atrial fibrillation (AF) is the most common cardiac arrhythmia. It has the tendency to evolve from short-lived episodes of arrhythmia (paroxysmal AF) to the development of persistent AF, which is continuously present. This pathology is associated with substantial atrial remodeling at different levels, of which structural remodeling is responsible for the slow progressive nature of AF. It is characterized by atrial dilatation and fibrosis. Treatment of AF is more successful in paroxysmal AF compared to persistent AF. It is therefore of clinical importance to understand the progressive nature of AF. The major aim of the project is to characterize the role of cardiac atrial fibroblasts in these processes. Fibroblasts are the dominant population among cardiac non-myocytes and play a central role in collagen deposition and matrix remodeling, but also participate in myocyte hypertrophic remodeling and dysfunction. Fibrosis is the result of excessive deposition of extracellular matrix proteins, mainly produced by differentiated fibroblasts. The role and phenotype of cardiac fibroblasts will be studied during the progression from paroxysmal to persistent AF and during structural reversibility after cardioversion to sinus rhythm in an animal model of AF.

Keywords:Cardiac fibroblasts, Atrial fibrillation, Fibrosis

Disciplines:Laboratory medicine, Palliative care and end-of-life care, Regenerative medicine, Other basic sciences, Other health sciences, Nursing, Other paramedical sciences, Other translational sciences, Other medical and health sciences