Abstract.
Electrical, contractile and structural remodeling have been characterized in atrial fibrillation (AF), and the latter is considered to be the major contributor to AF persistence. Recent data show that interstitial fibrosis can predispose to atrial conduction impairment and AF induction. The interplay between cardiac matrix metalloproteinases (MMPs) and their endogenous inhibitors, tissue inhibitors of MMPs (TIMPs), is thought to be critical in atrial extracellular matrix (ECM) metabolism. At the molecular level, angiotensin II, transforming growth factor-β1, inflammation and oxidative stress are particularly important for ECM dysregulation and atrial fibrotic remodeling in AF. Therefore, we review recent advances in the understanding of the atrial fibrotic process, the major downstream components in this remodeling process, and the expression and regulation of MMPs and TIMPs. We also describe the activation of bioactive molecules in both clinical studies and animal models to modulate MMPs and TIMPs and their effects on atrial fibrosis in AF.
Similar content being viewed by others
Author information
Authors and Affiliations
Corresponding author
Additional information
Received 5 September 2007; received after revision 22 December 2007; accepted 4 January 2008
Rights and permissions
About this article
Cite this article
Lin, CS., Pan, CH. Regulatory mechanisms of atrial fibrotic remodeling in atrial fibrillation. Cell. Mol. Life Sci. 65, 1489–1508 (2008). https://doi.org/10.1007/s00018-008-7408-8
Published:
Issue Date:
DOI: https://doi.org/10.1007/s00018-008-7408-8