While the exact mechanism underlying the development of AF has not been clearly established, atrial dilatation and fibrosis are known to influence a variety of biological processes, primarily through regulation of angiotensin II and related mediators (e.g. transforming growth factor [TGF]-β1, platelet derived growth factor [PDFG], connective tissue growth factor [CTGF]) [47]. Here, CCN2 is linked to atrial fibrillation.