A collaborative research team, led by Dr. Robert Rose, PhD, a professor in the departments of Cardiac Sciences and Physiology and Pharmacology at the Cumming School of Medicine, has been working tirelessly to better understand the biological mechanisms behind AF.
The team, which included a group of talented graduate students and postdoctoral fellows along with several other Libin Cardiovascular Institute researchers, recently published a study in Circulation: Arrhythmia and Electrophysiology, providing hope for the future.
The study reveals that a specific receptor in the heart, natriuretic peptide receptor B (NPR-B), plays a key role in sustaining normal heart rhythm. Impaired activity of this receptor puts people at high risk of developing AF.
"We found that individuals with AF have fewer NPR-B receptors and that when function of this receptor is impaired, you get inappropriate activity in the cells of the atria, which leads to calcium dysregulation and ultimately to triggering events that can initiate and sustain AF," says Rose.
The study built on the knowledge that the receptor is important in preventing overactivity of the sympathetic nervous system in the heart, a state that is known to increase the risk of AF.
According to Rose, the findings could lead to new preventive treatments for AF in the form of receptor-activating chemicals called NPR-B agonists.
"We know AF is highly prevalent and that current therapeutic approaches are often insufficient, so we need ways to target these protective pathways in the heart," says Rose. "Understanding how AF arises is critical in developing therapies that are specific to patient groups.
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