
Phenotypic markers of monocyte activation predict incident cardiovascular events above and beyond traditional CVD risk factors. This study extends results from animal and tissue models in which exposure to intermittent hypoxia induces NLRP3 inflammasome priming and activation. Although the authors make a compelling case that hypoxia, via HIF-1α, can be an important driver of NLRP3 inflammasome priming in OSA, other OSA-related exposures, such as sleep fragmentation, remain relevant be determined.
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