Abstract
Atrial fibrillation (AF) is regularly accompanied by cardiac fibrosis and concomitant heart failure. Due to the heterogeneous nature and complexity of fibrosis, the knowledge about the underlying mechanisms is limited, which prevents effective pharmacotherapy. A deeper understanding of cardiac fibroblasts is essential to meet this need. We previously described phenotypic and functional differences between atrial fibroblasts from patients in sinus rhythm and with AF. Herein, we established and characterized a novel human atrial fibroblast line, which displays typical fibroblast morphology and function comparable to primary cells but with improved proliferation capacity and low spontaneous myofibroblast differentiation. These traits make our model suitable for the study of fibrosis mechanisms and for drug screening aimed at developing effective antifibrotic pharmacotherapy.
Highlights
Atrial fibrillation (AF) is regularly accompanied by cardiac fibrosis and concomitant heart failure
A well-recognized concomitant of Cardiovascular diseases (CVD) is cardiac fibrosis [1], which is the structural manifestation of an imbalance in extracellular matrix (ECM) homeostasis
With nearly 45% of all deaths in the Western world attributable to fibroproliferative disease, the clinical relevance of fibrotic remodeling is enormous [3,4]. This is true in the case of atrial fibrosis, associated with a detrimental clinical outcome of highly abundant supraventricular arrhythmias like atrial fibrillation (AF) [5]
Summary
Atrial fibrillation (AF) is regularly accompanied by cardiac fibrosis and concomitant heart failure. We established and characterized a novel human atrial fibroblast line, which displays typical fibroblast morphology and function comparable to primary cells but with improved proliferation capacity and low spontaneous myofibroblast differentiation These traits make our model suitable for the study of fibrosis mechanisms and for drug screening aimed at developing effective antifibrotic pharmacotherapy. Myofibroblasts increase in size, commence expression of orderly arranged filaments of alpha-smooth muscle actin (aSMA), and become highly secretory, resulting in enhanced deposition of interstitial collagen as well as local enrichment of cytokines and other mediators of inflammation [11] This process is initially beneficial for wound healing, a prolonged presence of myofibroblasts is detrimental for physiological cardiac function [12]
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