Abstract
Pacemaker channels play a major role in the generation of sinoatrial rhythmic activity. However, their expression is not confined to specialized myocardial cells, such as primary and subsidiary pacemakers. Electrophysiological and molecular data collected over the last ten years have demonstrated that f-channels are also present in non-pacemaker cardiomyocytes, and become upregulated in cardiac hypertrophy and failure. Mislocalized expression and/or overexpression of f-channels are a consequence of electrophysiological remodeling and, from a clinical point of view, may represent an arrhythmogenic mechanism in heart failure, a condition associated with a high risk for sudden cardiac death. The potential arrhythmogenic role of I f and the availability of selective f-channel blockers cause I f to be a suitable therapeutic target in heart disease.
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.