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Atrial fibrillation (AF) as the most frequently occurring arrhythmia and a worldwide health care complication has persistently led to heart failure risk and overall mortality. This arrhythmic disorder has been assumed as a pure functional disorder for a long time, but in recent years significant structural basis of rapid and irregular electrical activity and contractile remodeling of the atria had been realized as underlying cause of this arrhythmia. The structural remodeling indicator in AF is atrial fibrosis development and progression. Galectin-3 (Gal-3), a novel pro-fibrotic molecule and a member of β-galactoside-binding lectin gene family consisting of two domains, namely an atypical N-terminal domain and a C-terminal carbohydrate recognition domain (CRD), is encoded by a single gene, LGALS3, which is located on chromosome 14, and contains six exons and five introns. Gal-3 has wide ranging functions, from playing a role in cell growth to a role in apoptotic pathways, and also Gal-3 is recruited in inflammatory and fibrotic conditions, such as cardiac fibrosis. Gal-3 recruits inflammatory cells in the pathogenesis of cardiac fibrosis which this in turn results in cellular proliferation and collagen deposition.

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Galectin-3 can doubtlessly be measured in blood circulation, and recent findings have indicated the prognostic value of galectin-3 in AF. The serum Gal-3 level is elevated in AF patients with preserved left ventricular function and in persistent AF patients in comparison with paroxysmal AF patients. In response to circulating cytokines such as IL-4 which is mainly secreted from T helper 2 (Th2) cells, and can aggravate Th2 over-expression, and differentiation of some macrophages to “alternative” subtype (M2). This type of macrophage is identified by the up-regulation of mannosereceptors, which are taking place in galectin-3 production and function pathways. This clue indicates that auto-immunological disorders may be the basis of AF.

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