دورية أكاديمية

Cardiomyocyte Deletion of Bmal1 Exacerbates QT- and RR-Interval Prolongation in Scn5a +/Δ KPQ Mice.

التفاصيل البيبلوغرافية
العنوان: Cardiomyocyte Deletion of Bmal1 Exacerbates QT- and RR-Interval Prolongation in Scn5a +/Δ KPQ Mice.
المؤلفون: Schroder, Elizabeth A., Wayland, Jennifer L., Samuels, Kaitlyn M., Shah, Syed F., Burgess, Don E., Seward, Tanya, Elayi, Claude S., Esser, Karyn A., Delisle, Brian P.
المصدر: Frontiers in Physiology; 6/24/2021, Vol. 12, p1-10, 10p
مصطلحات موضوعية: HEART beat, DELETION mutation, LONG QT syndrome, LABORATORY mice, MICE, ION channels, VENTRICULAR arrhythmia, 22Q11 deletion syndrome
مستخلص: Circadian rhythms are generated by cell autonomous circadian clocks that perform a ubiquitous cellular time-keeping function and cell type-specific functions important for normal physiology. Studies show inducing the deletion of the core circadian clock transcription factor Bmal1 in adult mouse cardiomyocytes disrupts cardiac circadian clock function, cardiac ion channel expression, slows heart rate, and prolongs the QT-interval at slow heart rates. This study determined how inducing the deletion of Bmal1 in adult cardiomyocytes impacted the in vivo electrophysiological phenotype of a knock-in mouse model for the arrhythmogenic long QT syndrome (Scn5a +/Δ KPQ ). Electrocardiographic telemetry showed inducing the deletion of Bmal1 in the cardiomyocytes of mice with or without the ΔKPQ- Scn5a mutation increased the QT-interval at RR-intervals that were ≥130 ms. Inducing the deletion of Bmal1 in the cardiomyocytes of mice with or without the ΔKPQ- Scn5a mutation also increased the day/night rhythm-adjusted mean in the RR-interval, but it did not change the period, phase or amplitude. Compared to mice without the ΔKPQ- Scn5a mutation, mice with the ΔKPQ- Scn5a mutation had reduced heart rate variability (HRV) during the peak of the day/night rhythm in the RR-interval. Inducing the deletion of Bmal1 in cardiomyocytes did not affect HRV in mice without the ΔKPQ- Scn5a mutation, but it did increase HRV in mice with the ΔKPQ- Scn5a mutation. The data demonstrate that deleting Bmal1 in cardiomyocytes exacerbates QT- and RR-interval prolongation in mice with the ΔKPQ- Scn5a mutation. [ABSTRACT FROM AUTHOR]
Copyright of Frontiers in Physiology is the property of Frontiers Media S.A. and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)
قاعدة البيانات: Complementary Index
الوصف
تدمد:1664042X
DOI:10.3389/fphys.2021.681011