Abstract
Non-alcoholic fatty liver disease (NAFLD) is a chronic liver disease characterized by lipid accumulation in hepatocytes in the absence of excessive alcohol consumption. The global prevalence of NAFLD is constantly increasing. NAFLD is a disease spectrum comprising distinct stages with different prognoses. Non-alcoholic steatohepatitis (NASH) is a progressive condition, characterized by liver inflammation and hepatocyte ballooning, with or without fibrosis. The natural history of NAFLD is negatively influenced by NASH onset and by the progression towards advanced fibrosis. Pathogenetic mechanisms and cellular interactions leading to NASH and fibrosis involve hepatocytes, liver macrophages, myofibroblast cell subpopulations, and the resident progenitor cell niche. These cells are implied in the regenerative trajectories following liver injury, and impairment or perturbation of these mechanisms could lead to NASH and fibrosis. Recent evidence underlines the contribution of extra-hepatic organs/tissues (e.g., gut, adipose tissue) in influencing NASH development by interacting with hepatic cells through various molecular pathways. The present review aims to summarize the role of hepatic parenchymal and non-parenchymal cells, their mutual influence, and the possible interactions with extra-hepatic tissues and organs in the pathogenesis of NAFLD.
Highlights
Non-alcoholic fatty liver disease (NAFLD) is a chronic liver disease characterized by hepatic fat accumulation in the absence of excessive alcohol consumption, and defined by the presence of steatosis in at least 5% of hepatocytes [1]
A mathematical model was built to understand how the disease burden associated with NAFLD and non-alcoholic steatohepatitis (NASH) will change over time, and the results suggest an increase in the number of cases of advanced liver disease and in liver-related mortality in the coming years, in concert with a global pandemic of obesity [5]
Characterizes both adult [144] and pediatric [110] populations affected by advanced stages
Summary
Non-alcoholic fatty liver disease (NAFLD) is a chronic liver disease characterized by hepatic fat accumulation in the absence of excessive alcohol consumption, and defined by the presence of steatosis in at least 5% of hepatocytes [1]. The term NASH covers a wide spectrum of disease severity, including progressive fibrosis and cirrhosis Both NAFL and NASH can cause hepatocellular carcinoma (HCC) in the presence or absence of liver fibrosis and cirrhosis; in these patients, HCC incidence can vary from 2.4%. Cells 2020, 9, 590 indication for liver transplantation in the USA [4] Both NAFL and NASH are becoming increasingly prevalent as the epidemics of obesity and diabetes continue to increase. The prevalence of children obesity is increasing in most regions of the world [7,8], causing a rise in the risk of developing chronic diseases, such as type 2 diabetes, cardiovascular disease, and NAFLD [9]. The present review aims to summarize the role of hepatic parenchymal and non-parenchymal cells and their cross-talks in the pathogenesis of NAFLD, and the possible interactions with extra-hepatic tissues/organs
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