Table of Contents Author Guidelines Submit a Manuscript
Mediators of Inflammation
Volume 2015 (2015), Article ID 815721, 10 pages
http://dx.doi.org/10.1155/2015/815721
Review Article

OSAS-Related Inflammatory Mechanisms of Liver Injury in Nonalcoholic Fatty Liver Disease

1Gradenigo Hospital, University of Turin, Corso Regina Margherita, 10132 Turin, Italy
2Department of Medical Sciences, San Giovanni Battista Hospital, University of Turin, Corso Bramante 14, 10124 Turin, Italy
3Hepato-Metabolic Disease Unit, Bambino Gesù Children’s Hospital and IRCCS, S. Onofrio Square 4, 00165 Rome, Italy
4Pneumology Unit, Sleep and Noninvasive Ventilation Laboratory, Bambino Gesù Children’s Hospital and IRCCS, S. Onofrio Square 4, 00165 Rome, Italy

Received 31 July 2014; Revised 22 September 2014; Accepted 7 October 2014

Academic Editor: Leila Kheirandish-Gozal

Copyright © 2015 Elena Paschetta et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Obstructive sleep apnoea syndrome (OSAS) is a common sleep disorder, affecting over 4% of the general population, and is associated with metabolic syndrome and cardiovascular disease, independent of obesity and traditional risk factors. OSAS has been recently connected to nonalcoholic fatty liver disease (NAFLD), the most common chronic liver disease in the world, which can be found in 30% of the general adult population. Several studies suggest that the chronic intermittent hypoxia (CIH) of OSAS patients may per se trigger liver injury, inflammation, and fibrogenesis, promoting NAFLD development and the progression from steatosis to steatohepatitis, cirrhosis, and hepatocellular carcinoma. In NAFLD patients, liver disease may be caused by hypoxia both indirectly by promoting inflammation and insulin resistance and directly by enhancing proinflammatory cytokine production and metabolic dysregulation in liver cells. In this review, we focus on molecular mechanisms linking OSAS to NAFLD, including hypoxia inducible factor (HIF), nuclear factor kappa B (NF-κB), YKL-40, unfolded protein response, and hypoxic adipose tissue inflammation, which all could provide novel potential therapeutic approaches for the management of NAFLD patients with OSAS.