Atrial fibrillation (AF) is associated with profound structural and functional changes in the atrium. Inflammation mediated atrial fibrosis is one of the key mechanisms in the pathogenesis of AF. The collagen deposition in extracellular matrix (ECM) is mainly mediated by transforming growth factor β1 (TGF-β1) which promotes AF via controlling smads mediated-collagen gene transcription and regulating the balance of metalloproteinases (MMPs)/ tissue inhibitor of metalloproteinases (TIMPs). Although many processes can alter atrial properties and promote AF, animal models and clinical studies have provided insights into 2 major forms of atrial remodeling: Atrial tachycardia remodeling (ATR), which occurs with rapid atrial tachyarrhythmia's such as AF and atrial flutter, and atrial structural remodeling (ASR), which is associated with CHF and other fibrosis-promoting conditions. The mechanism of atrial remodeling such as atrial enlargement, ultra-structural changes of atrial muscle tissue and myocardial interstitial fibrosis in AF is still unclear. At present, many studies focus on calcium overload, renin angiotensin aldosterone system and transforming growth factor β1, that effect on atrial structural remodeling. Recent experimental studies and clinical investigations have provided structural remodeling is important contributor to the AF. This paper reviews the current understanding of the progresses about mechanism of atrial structural remodeling, and highlights the potential therapeutic approaches aimed at attenuating structural remodeling to prevent AF. Now some recent advancements of this area are reviewed in this paper.
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