Disrupting circadian rhythms, which change naturally on a 24-hour cycle, has been implicated in heart disease, but it is unclear how it leads to the condition. A research team at Baylor College of Medicine and collaborating institutions investigated the function of the protein Rev-erbα/β, a key component of the circadian clock, on heart disease development in animal models and human patients.
The team reports in the journal Circulation that Rev-erbα/β in cardiomyocytes mediates a normal metabolic rhythm that enables the cells to prefer lipids as a source of energy during the animal’s resting time, daytime for mice. Removing Rev-erbα/β disrupts this rhythm, reduces the cardiomyocytes’ ability to use lipids in the resting time and leads to progressive dilated cardiomyopathy and lethal heart failure.
“We studied how the Rev-erbα/β gene influenced the metabolism of the heart by…
