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The contribution of obstructive sleep apnoea to the pathophysiology of non-alcoholic fatty liver disease (NAFLD). Following the first ‘hit’ of fatty liver deposition, the chronic intermittent hypoxia of obstructive sleep apnoea contributes to endothelial damage that contributes to the fibrotic change seen in NAFLD. ROS, reactive oxygen species; HIF 1-alpha, hypoxia inducible factor 1-alpha; LOX-1, lectin-like oxidized low-density lipoprotein receptor-1.
