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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