A novel murine model of atrial fibrillation by diphtheria toxin-induced injury.
amiodarone
atrial fibrillation
diphtheria toxin
non-genetic cause
sarcolipin (SLN)
Journal
Frontiers in physiology
ISSN: 1664-042X
Titre abrégé: Front Physiol
Pays: Switzerland
ID NLM: 101549006
Informations de publication
Date de publication:
2022
2022
Historique:
received:
24
06
2022
accepted:
04
08
2022
entrez:
17
11
2022
pubmed:
18
11
2022
medline:
18
11
2022
Statut:
epublish
Résumé
The treatment of atrial fibrillation (AF) continues to be a significant clinical challenge. While genome-wide association studies (GWAS) are beginning to identify AF susceptibility genes (Gudbjartsson et al., Nature, 2007, 448, 353-357; Choi et al., Circ. Res., 2020, 126, 200-209; van Ouwerkerk et al., Circ. Res., 2022, 127, 229-243), non-genetic risk factors including physical, chemical, and biological environments remain the major contributors to the development of AF. However, little is known regarding how non-genetic risk factors promote the pathogenesis of AF (Weiss et al., Heart Rhythm, 2016, 13, 1868-1877; Chakraborty et al., Heart Rhythm, 2020, 17, 1,398-1,404; Nattel et al., Circ. Res., 2020, 127, 51-72). This is, in part, due to the lack of a robust and reliable animal model induced by non-genetic factors. The currently available models using rapid pacing protocols fail to generate a stable AF phenotype in rodent models, often requiring additional genetic modifications that introduce potential sources of bias (Schüttler et al., Circ. Res., 2020, 127, 91-110). Here, we report a novel murine model of AF using an inducible and tissue-specific activation of diphtheria toxin (DT)-mediated cellular injury system. By the tissue-specific and inducible expression of human HB-EGF in atrial myocytes, we developed a reliable, robust and scalable murine model of AF that is triggered by a non-genetic inducer without the need for AF susceptibility gene mutations.
Identifiants
pubmed: 36388109
doi: 10.3389/fphys.2022.977735
pii: 977735
pmc: PMC9659601
doi:
Types de publication
Journal Article
Langues
eng
Pagination
977735Subventions
Organisme : NHLBI NIH HHS
ID : R01 HL142801
Pays : United States
Informations de copyright
Copyright © 2022 Trieu, Mach, Bunn, Huang, Huang, Chow, Nakano, Fajardo, Touma, Ren, Wang and Nakano.
Déclaration de conflit d'intérêts
The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
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