Calcium handling abnormalities increase arrhythmia susceptibility in DMSXL myotonic dystrophy type 1 mice
The DMSXL mouse model of DM1 exhibited enhanced arrhythmogenicity associated with abnormal intracellular calcium handling due to hyperphosphorylation of RyR2, pointing to RyR2 as a potential new therapeutic target in DM1 treatment.
Authors
- Mohamed Chahine (ORCID: https://orcid.org/0000-0002-9500-2839)
- Mohamed Boutjdir (ORCID: https://orcid.org/0000-0002-6068-223X)
- Jean‐Baptiste Reisqs (ORCID: https://orcid.org/0000-0001-9881-6670)
- Vamsi Krishna Murthy Ginjupalli (ORCID: https://orcid.org/0000-0002-5022-1683)
- Jack Puymirat (ORCID: https://orcid.org/0000-0002-6169-2931)
- Geneviève Gourdon (ORCID: https://orcid.org/0000-0002-3319-1347)
- Nabil El‐Sherif (ORCID: https://orcid.org/0000-0001-7233-5991)
- Yvonne Sleiman (ORCID: https://orcid.org/0000-0002-1550-8945)
- Michael Cupelli (ORCID: https://orcid.org/0000-0001-8985-2290)
Institutions
- Inserm (FR)
- VA NY Harbor Healthcare System (US)
- Sorbonne Université (FR)
- Institut de Myologie (FR)
- Institut Universitaire en Santé Mentale de Québec (CA)
- Université Laval (CA)
- Centre de Recherche en Myologie
Publication Details
- Journal
- Biomedicine & Pharmacotherapy
- Published
- 2024-10-17
- DOI
- https://doi.org/10.1016/j.biopha.2024.117562
- Citations
- 4
- Primary Topic
- Genetic Neurodegenerative Diseases
- Type
- article
- Field-Weighted Citation Impact
- 1.07
Funders
- U.S. Department of Defense
- U.S. Department of Veterans Affairs
- Biomedical Laboratory Research and Development, VA Office of Research and Development
- Canadian Institutes of Health Research
- National Heart, Lung, and Blood Institute