Non-alcoholic fatty liver disease: Immunological mechanisms and current treatments

Figure 2 Overview of mitochondrial dynamics in non-alcoholic fatty liver disease. The accumulation of triglycerides and free fatty acids (FFAs) in the liver are converted to fatty acyl-CoA, which is then transported to the mitochondria for β-oxidation, generating acetyl-CoA. However, increased accumulation of FFA can cause insufficient hepatic β-oxidation, triggering inflammation and oxidative stress. Acetyl-CoA enters the mitochondrial tricarboxylic acid cycle allowing continuation of gluconeogenesis. The by-product nicotinamide adenine dinucleotide, produced though β-oxidation are transported to the electron transport chain (ETC) for oxidative phosphorylation. Disruption and dysfunction of the ETC can cause electron leakage and hepatocyte damage leading to reactive oxygen species production and oxidative stress. Accumulation of FFAs can cause mitochondrial damage, resulting in increased mitochondrial fission and degradation via mitophagy processes (created with BioRender.com). ROS: Reactive oxygen species; NADH: Nicotinamide adenine dinucleotide; TCA: Tricarboxylic acid; ADP: Adenosine diphosphate; ATP: Adenosine triphosphate.