OSAS-Related Inflammatory Mechanisms of Liver Injury in Nonalcoholic Fatty Liver Disease
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 di...
Saved in:
| Main Authors: | , , , , , , |
|---|---|
| Format: | Article |
| Language: | English |
| Published: |
Wiley
2015-01-01
|
| Series: | Mediators of Inflammation |
| Online Access: | http://dx.doi.org/10.1155/2015/815721 |
| Tags: |
Add Tag
No Tags, Be the first to tag this record!
|
| _version_ | 1832566989538721792 |
|---|---|
| author | Elena Paschetta Paola Belci Anna Alisi Daniela Liccardo Renato Cutrera Giovanni Musso Valerio Nobili |
| author_facet | Elena Paschetta Paola Belci Anna Alisi Daniela Liccardo Renato Cutrera Giovanni Musso Valerio Nobili |
| author_sort | Elena Paschetta |
| collection | DOAJ |
| description | 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. |
| format | Article |
| id | doaj-art-c0d618facfba41018a92f3c88804247f |
| institution | Kabale University |
| issn | 0962-9351 1466-1861 |
| language | English |
| publishDate | 2015-01-01 |
| publisher | Wiley |
| record_format | Article |
| series | Mediators of Inflammation |
| spelling | doaj-art-c0d618facfba41018a92f3c88804247f2025-02-03T01:02:40ZengWileyMediators of Inflammation0962-93511466-18612015-01-01201510.1155/2015/815721815721OSAS-Related Inflammatory Mechanisms of Liver Injury in Nonalcoholic Fatty Liver DiseaseElena Paschetta0Paola Belci1Anna Alisi2Daniela Liccardo3Renato Cutrera4Giovanni Musso5Valerio Nobili6Gradenigo Hospital, University of Turin, Corso Regina Margherita, 10132 Turin, ItalyDepartment of Medical Sciences, San Giovanni Battista Hospital, University of Turin, Corso Bramante 14, 10124 Turin, ItalyHepato-Metabolic Disease Unit, Bambino Gesù Children’s Hospital and IRCCS, S. Onofrio Square 4, 00165 Rome, ItalyHepato-Metabolic Disease Unit, Bambino Gesù Children’s Hospital and IRCCS, S. Onofrio Square 4, 00165 Rome, ItalyPneumology Unit, Sleep and Noninvasive Ventilation Laboratory, Bambino Gesù Children’s Hospital and IRCCS, S. Onofrio Square 4, 00165 Rome, ItalyGradenigo Hospital, University of Turin, Corso Regina Margherita, 10132 Turin, ItalyHepato-Metabolic Disease Unit, Bambino Gesù Children’s Hospital and IRCCS, S. Onofrio Square 4, 00165 Rome, ItalyObstructive 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.http://dx.doi.org/10.1155/2015/815721 |
| spellingShingle | Elena Paschetta Paola Belci Anna Alisi Daniela Liccardo Renato Cutrera Giovanni Musso Valerio Nobili OSAS-Related Inflammatory Mechanisms of Liver Injury in Nonalcoholic Fatty Liver Disease Mediators of Inflammation |
| title | OSAS-Related Inflammatory Mechanisms of Liver Injury in Nonalcoholic Fatty Liver Disease |
| title_full | OSAS-Related Inflammatory Mechanisms of Liver Injury in Nonalcoholic Fatty Liver Disease |
| title_fullStr | OSAS-Related Inflammatory Mechanisms of Liver Injury in Nonalcoholic Fatty Liver Disease |
| title_full_unstemmed | OSAS-Related Inflammatory Mechanisms of Liver Injury in Nonalcoholic Fatty Liver Disease |
| title_short | OSAS-Related Inflammatory Mechanisms of Liver Injury in Nonalcoholic Fatty Liver Disease |
| title_sort | osas related inflammatory mechanisms of liver injury in nonalcoholic fatty liver disease |
| url | http://dx.doi.org/10.1155/2015/815721 |
| work_keys_str_mv | AT elenapaschetta osasrelatedinflammatorymechanismsofliverinjuryinnonalcoholicfattyliverdisease AT paolabelci osasrelatedinflammatorymechanismsofliverinjuryinnonalcoholicfattyliverdisease AT annaalisi osasrelatedinflammatorymechanismsofliverinjuryinnonalcoholicfattyliverdisease AT danielaliccardo osasrelatedinflammatorymechanismsofliverinjuryinnonalcoholicfattyliverdisease AT renatocutrera osasrelatedinflammatorymechanismsofliverinjuryinnonalcoholicfattyliverdisease AT giovannimusso osasrelatedinflammatorymechanismsofliverinjuryinnonalcoholicfattyliverdisease AT valerionobili osasrelatedinflammatorymechanismsofliverinjuryinnonalcoholicfattyliverdisease |