Abstract
Myocarditis underlies 42% of sudden cardiac death in young adults, yet viral arrhythmogenic mechanisms remain elusive. Adenovirus is a leading cause but species-specificity has limited disease modeling in mice. Gap junctions, composed primarily of connexin43 (Cx43), enable electrical impulse propagation in the heart. Changes in Cx43 expression, localization, and/or function cause arrhythmias. Gap junctions propagate innate and adaptive antiviral responses, and our prior work has demonstrated that Cx43 expression and function are reduced during human adenoviral infection.
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.