| Literature DB >> 26847547 |
Marina Nati1, David Haddad1, Andreas L Birkenfeld2,3,4,5, Christian A Koch6, Triantafyllos Chavakis1,3,4,7, Antonios Chatzigeorgiou8,9,10,11.
Abstract
The low grade inflammatory state present in obesity promotes the progression of Non-Alcoholic Fatty Liver Disease (NAFLD). In Non-Alcoholic Steatohepatitis (NASH), augmented hepatic steatosis is accompanied by aberrant intrahepatic inflammation and exacerbated hepatocellular injury. NASH is an important disorder and can lead to fibrosis, cirrhosis and even neoplasia. The pathology of NASH involves a complex network of mechanisms, including increased infiltration of different subsets of immune cells, such as monocytes, T-lymphocytes and neutrophils, to the liver, as well as activation and in situ expansion of liver resident cells such as Kupffer cells or stellate cells. In this review, we summarize recent advances regarding understanding the role of the various cells of the innate and adaptive immunity in NASH development and progression, and discuss possible future therapeutic options and tools to interfere with disease progression.Entities:
Keywords: Hepatic stellate cells (HSC); Kupffer cells; Non-alcoholic steatohepatitis (NASH); Obesity; Steatosis; T-regulatory cells (Tregs)
Mesh：
Year: 2016 PMID： 26847547 DOI： 10.1007/s11154-016-9339-2
Source DB: PubMed Journal: Rev Endocr Metab Disord ISSN： 1389-9155 Impact factor: 6.514