Publication Date
6-1-2023
Journal
Mammalian Genome
DOI
10.1007/s00335-022-09964-x
PMID
36173465
PMCID
PMC10898345
PubMedCentral® Posted Date
2-27-2024
PubMedCentral® Full Text Version
Author MSS
Published Open-Access
yes
Keywords
Animals, Mice, Atrial Fibrillation, Disease Models, Animal, Disease Progression
Abstract
Atrial fibrillation (AF) is the most common arrhythmia in adults, with a prevalence increasing with age. Current clinical management of AF is focused on tertiary prevention (i.e., treating the symptoms and sequelae) rather than addressing the underlying molecular pathophysiology. Robust animal models of AF, particularly those that do not require supraphysiologic stimuli to induce AF (i.e., showing spontaneous AF), enable studies that can uncover the underlying mechanisms of AF. Several mouse models of AF have been described to exhibit spontaneous AF, but pathophysiologic drivers of AF differ among models. Here, we describe relevant AF mechanisms and provide an overview of large and small animal models of AF. We then provide an in-depth review of the spontaneous mouse models of AF, highlighting the relevant AF mechanisms for each model.
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