A novel murine model of atrial fibrillation by diphtheria toxin-induced injury
Frontiers in Physiology · 2022
A new mouse model reliably produces atrial fibrillation through a controlled, non-genetic injury to atrial heart cells.
Research question
Can a robust rodent model of atrial fibrillation be created without relying on susceptibility-gene mutations?
Clinical & scientific significance
Provides a tool for studying how non-genetic injury promotes atrial fibrillation, avoiding biases of genetically modified pacing models.
Key findings reported in the paper
- The approach produced a reliable, robust and scalable murine model of atrial fibrillation triggered by a non-genetic inducer.
Objectives
To develop an inducible, tissue-specific injury model of atrial fibrillation.
Methods
Inducible expression of human HB-EGF (the diphtheria-toxin receptor) in atrial myocytes, followed by diphtheria toxin to cause targeted cellular injury.
This summary is based only on the published abstract.
A non-genetic model of atrial fibrillation
01
Targeted receptor
Human HB-EGF is expressed only in atrial heart-muscle cells.
02
Controlled injury
An inducible trigger causes injury confined to those cells.
03
Rhythm disorder
The animals develop atrial fibrillation without susceptibility-gene mutations.
04
A reliable tool
A robust, scalable model for studying non-genetic causes.
Read the publication
Authors
Trieu T, Mach P, Bunn K, Huang V, Huang J, Chow C, Nakano H, Fajardo VM, Touma M, Ren S, Wang Y, Nakano A
Citation
A novel murine model of atrial fibrillation by diphtheria toxin-induced injury. Front Physiol. 2022; 13:977735. doi:10.3389/fphys.2022.977735. PMID: 36388109.
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