Abstract
We read with great interest the paper by Herrmann et al .1 describing the effects of inducible HCN4-positive cell deletion in the mouse. This novel study using Cre- lox P adds to their previous work using this system to knock down HCN4 expression in adult mice and is a valuable contribution to unravelling the complexities of sinoatrial node (SAN) function and disease.1 The authors claim that their DTA/KiT mouse represents an accurate analogue of human sick sinus syndrome (SSS). For example, in the DTA/KiT mouse, following HCN4-positive cell deletion, there is a marked cell loss and fibrosis in the SAN. Literature is cited that alleges age-related degenerative fibrosis is the primary pathological mechanism of SSS. However, careful analysis of the published literature casts doubt on …
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: 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.
