Cell-type specific role of autophagy in the liver and its implications in non-alcoholic fatty liver disease

Figure 1 Cell-specific effects of autophagy modulation on liver pathology in non-alcoholic fatty liver disease. A: Hepatocytes: Loss of autophagy results in accumulation of oxidative protein and lipid adducts, triacylglycerols and defective mitochondria; B: Macrophage/Kupffer cells: Inhibition of macrophage autophagy results in increased generation of pro-inflammatory M1 polarized macrophages, which increases inflammation during non-alcoholic fatty liver disease (NAFLD)/non-alcoholic steatohepatitis progression; C: Liver sinusoidal endothelial cells (LSECs): Loss of autophagy in LSECs results in cellular stress and loss of cellular integrity, resulting in increased NAFLD progression; D: Hepatic stellate cells (HSCs): The effect of autophagy on HSCs is conflicting, with some studies demonstrating its anti-fibrotic action while others support its pro-fibrotic action by regulating the transformation of quiescent HSCs into collagen-secreting myofibroblasts. HSCs: Hepatic stellate cells.