Genetic–Genomic Insights Into the Metabolic Determinants of Spontaneous Atrial Fibrillation
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Atrial fibrillation (AF) is a complex aging-associated disease with multiple causes and inadequate treatment options. Beyond anticoagulants, the pharmacological treatments for AF have had limited efficacy and a potential for significant side effects. A major challenge in developing new drugs to treat or prevent AF has been the lack of suitable animal models of spontaneous AF.1 Studies from Müller et al2 have shown that overexpression of the cAMP response element modulator (CREM) in mice led to atrial enlargement with atrial and ventricular hypertrophy, leading to spontaneous AF and premature death. In additional studies of this model, changes in calcium cycling that promoted hypertrophy of atrial myocytes and chamber dilatation were shown to precede the development of electrical heterogeneity, conduction slowing, and atrial ectopy.3 Complementary studies in human atrial tissues and in other animal models of AF have led to an improved understanding of the role of abnormal calcium cycling and metabolism in the development of atrial cardiomyopathies as a substrate for AF.4
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