Brian P. Delisle, PhD
Connect
(859) 323-2797bpdeli00@uky.edu
Positions
- Professor, Department of Physiology
- Director of Education, Department of Physiology
College Unit(s)
Other Affiliation(s)
- CVRC - Affiliated Faculty
Biography and Education
Biography
Our research investigates how circadian rhythms, genetics, and environmental factors regulate cardiac ion channels and influence arrhythmia susceptibility. We use molecular, electrophysiological, and in vivo approaches to define how daily rhythms in light and feeding affect cardiac excitability and long QT syndrome risk. We also study how genetic variants alter ion channel function. In addition to research, I serve as an Associate Editor for the American Journal of Physiology-Cell Physiology and as a Review Editor for The Journal of Physiology. I also serve as the course director for our undergraduate physiology courses, PGY 206 and 207, and I am our department’s Education Director.
Education
Ph.D. (Physiology and Biophysics) University of Kentucky, Lexington, KY, 2001.
Research
Our research program focuses on understanding how circadian rhythms, genetic variation, and environmental factors interact to regulate cardiac ion channels and influence susceptibility to arrhythmias and sudden cardiac death.
I earned my Ph.D. in Physiology and Biophysics from the University of Kentucky. I then joined Dr. Craig January’s laboratory at the University of Wisconsin–Madison, where my work focused on the biophysical properties of cardiac potassium channels, particularly KCNQ1 and KCNH2 (hERG), and their roles in congenital long QT syndrome (LQTS). After returning to the University of Kentucky, our lab has continued to explore how the function and regulation of cardiac ion channels contribute to both inherited and acquired arrhythmia syndromes.
A significant focus of our current work is understanding how circadian rhythms and daily behavioral cycles influence cardiac electrophysiology. Circadian rhythms are generated by a molecular clock that operates on a roughly 24-hour cycle, synchronizing cellular and systemic physiology with environmental cues such as light and feeding. We are testing the hypothesis that disruptions in this clock can modify arrhythmia susceptibility. Using control and transgenic mouse models, we are defining how genetic and environmental misalignment of circadian rhythms affects ion channel expression, cardiac repolarization, and arrhythmia risk. This work aims to uncover gene-environment-behavior interactions that influence the timing and severity of life-threatening cardiac events, revealing new mechanisms by which ion channel function is regulated across the day-night cycle.
In parallel, we are also addressing the challenge of interpreting genetic variants of uncertain significance (VUS) identified in LQTS-linked genes. By combining electrophysiological, molecular, and computational approaches, our goal is to develop efficient, mechanistically grounded strategies for determining whether specific variants alter ion channel function and contribute to disease.
Together, these efforts aim to connect circadian biology, genetics, and physiology to better understand and ultimately prevent sudden cardiac death.