Sleep Apnea May Trigger Arterial Plaques Through Key Receptor

A new study has uncovered a potential link between obstructive sleep apnea and the development of arterial plaques. Researchers at the University of California, San Diego (UCSD) found that the FXR receptor plays a key role in this process. Their findings suggest a possible way to reduce heart disease risk in people with the condition. Obstructive sleep apnea causes repeated breathing interruptions during sleep. These pauses cut off oxygen to tissues and disrupt bile acids, which can harm metabolic health. The UCSD team discovered that the FXR receptor drives the buildup of fatty plaques in arteries when sleep apnea occurs.

In experiments, mice without the FXR receptor showed far fewer plaques in the aorta and aortic arch, even when exposed to simulated sleep apnea. Removing the receptor also protected their gut microbiome and metabolic profile from damage. However, while plaque formation decreased in most arteries, fatty deposits remained in the pulmonary artery.

The team now plans to compare these results with human clinical data. Follow-up trials will test whether targeting the FXR receptor could help prevent heart disease in sleep apnea patients. The study highlights a direct connection between sleep apnea, the FXR receptor, and arterial plaque formation. Future research will explore whether blocking this receptor could reduce cardiovascular risks. If confirmed in humans, the findings may lead to new treatments for sleep apnea-related heart conditions.