Connexin-43 Restoration Alleviates Desmosomal Arrhythmogenic Cardiomyopathy
By using mouse and human models of desmosomal ACM harboring different mutational backgrounds, we show the sufficiency of Cx43 gene therapy and its restoration to modify and alleviate ACM deficits. These data suggest that noncanonical functions of Cx43, including mechanical modulation and reassembly of the desmosome, are a therapeutic target with the potential to treat diverse ACM populations.
Authors
- Farah Nadia Sheikh
- Cassiano Carromeu (ORCID: https://orcid.org/0000-0002-7570-2213)
- R. J. P. Lyon (ORCID: https://orcid.org/0000-0003-3776-2087)
- I. Karakikes
- Fabian Zanella (ORCID: https://orcid.org/0000-0001-6985-4221)
- Alysson Renato Muotri (ORCID: https://orcid.org/0000-0003-0867-2875)
- Matthew W. Ellis (ORCID: https://orcid.org/0000-0002-7407-4374)
- Erika J. Gutiérrez-Lara (ORCID: https://orcid.org/0000-0003-1780-7487)
- Joel W. Martin (ORCID: https://orcid.org/0000-0001-5607-3338)
- Yusu Gu
- Valeria Mezzano
- Melvin Scheinman
- Kirk L. Peterson
- William H. Bradford
- Charlize Duron
- Kyohei Fujita
- Jing Zhang
- Tsui-Min Wang
Institutions
- University of California, San Francisco (US)
- Population Health Research Institute (CA)
- University of Illinois Chicago (US)
- San Diego Cardiac Center (US)
- Stanford University (US)
Publication Details
- Journal
- Circulation Heart Failure
- Published
- 2026-01-26
- DOI
- https://doi.org/10.1161/circheartfailure.125.013801
- Citations
- 1
- Primary Topic
- Cardiovascular Effects of Exercise
- Type
- article
- Field-Weighted Citation Impact
- 30.07