The mechanism by which sleep affects the risk of atherosclerosis (the build-up of plaques inside arteries) in mice is described in a paper published online in Nature this week. Although these findings need to be replicated in humans, they suggest a causal relationship between adequate sleep and cardiovascular health.
Atherosclerosis is a common cause of heart disease. Reduced or poor-quality sleep has been associated with a variety of health conditions, including an increased risk of heart disease. However, little is known about the cellular and molecular mechanisms by which sleep may affect cardiovascular health.
Filip Swirski and colleagues investigated the effects of chronic sleep fragmentation (interrupted or insufficient sleep) in atherosclerosis-prone genetically modified mice. The authors report that mice subjected to long-term sleep fragmentation were more anxious, produced more inflammatory cells, and developed larger atherosclerotic lesions than controls. The mice also produced less hypocretin (a neuropeptide that regulates wakefulness) in the lateral hypothalamus region of the brain.
The authors report that hypocretin controls the production of blood cells, including immune cells, via a signalling protein called CSF1. They conclude that the observed increase in immune cell production and accelerated development of atherosclerosis in sleep-deprived mice was caused by the reduced hypocretin and increased CSF1 levels. Restoring hypocretin levels in these mice reduced atherosclerosis. The authors suggest that undisturbed sleep maintains appropriate hypocretin release from the hypothalamus and offers a protective effect on cardiovascular health.
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