Your browser doesn't support javascript.
loading
A novel murine model of atrial fibrillation by diphtheria toxin-induced injury.
Trieu, Theresa; Mach, Philbert; Bunn, Kaitlyn; Huang, Vincent; Huang, Jamie; Chow, Christine; Nakano, Haruko; Fajardo, Viviana M; Touma, Marlin; Ren, Shuxun; Wang, Yibin; Nakano, Atsushi.
Afiliación
  • Trieu T; Department of Molecular, Cell, Developmental Biology, School of Life Science, University of California, Los Angeles, Los Angeles, CA, United States.
  • Mach P; Department of Molecular, Cell, Developmental Biology, School of Life Science, University of California, Los Angeles, Los Angeles, CA, United States.
  • Bunn K; Department of Molecular, Cell, Developmental Biology, School of Life Science, University of California, Los Angeles, Los Angeles, CA, United States.
  • Huang V; Department of Molecular, Cell, Developmental Biology, School of Life Science, University of California, Los Angeles, Los Angeles, CA, United States.
  • Huang J; Department of Molecular, Cell, Developmental Biology, School of Life Science, University of California, Los Angeles, Los Angeles, CA, United States.
  • Chow C; Department of Molecular, Cell, Developmental Biology, School of Life Science, University of California, Los Angeles, Los Angeles, CA, United States.
  • Nakano H; Department of Molecular, Cell, Developmental Biology, School of Life Science, University of California, Los Angeles, Los Angeles, CA, United States.
  • Fajardo VM; Department of Pediatrics, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA, United States.
  • Touma M; Department of Pediatrics, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA, United States.
  • Ren S; Departments of Anesthesiology, Physiology, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA, United States.
  • Wang Y; Departments of Anesthesiology, Physiology, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA, United States.
  • Nakano A; Department of Medicine, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA, United States.
Front Physiol ; 13: 977735, 2022.
Article en En | MEDLINE | ID: mdl-36388109
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.
Palabras clave
Texto completo
Imprimir
XML
PubMed Links
Buscar en Google

Texto completo: 1 Colección: 01-internacional Banco de datos: MEDLINE Tipo de estudio: Guideline / Prognostic_studies Idioma: En Revista: Front Physiol Año: 2022 Tipo del documento: Article País de afiliación: Estados Unidos
Texto completo
Imprimir
XML
PubMed Links
Buscar en Google

Texto completo: 1 Colección: 01-internacional Banco de datos: MEDLINE Tipo de estudio: Guideline / Prognostic_studies Idioma: En Revista: Front Physiol Año: 2022 Tipo del documento: Article País de afiliación: Estados Unidos