Innate Immune System in the Pathogenesis of Non-Alcoholic Fatty Liver Disease

Non-alcoholic fatty liver disease (NAFLD) is a prevalent condition characterized by lipid accumulation in hepatocytes with low alcohol consumption. The development of sterile inflammation, which occurs in response to a range of cellular stressors or injuries, has been identified as a major contributor to the pathogenesis of NAFLD. Recent studies of the pathogenesis of NAFLD reported the newly developed roles of damage-associated molecular patterns (DAMPs). These molecules activate pattern recognition receptors (PRRs), which are placed in the infiltrated neutrophils, dendritic cells, monocytes, or Kupffer cells. DAMPs cause the activation of PRRs, which triggers a number of immunological responses, including the generation of cytokines that promote inflammation and the localization of immune cells to the site of the damage. This review provides a comprehensive overview of the impact of DAMPs and PRRs on the development of NAFLD.

Automated summary

Non-alcoholic fatty liver disease (NAFLD) is a common condition characterized by lipid accumulation in the liver cells with low alcohol consumption. Recent studies have identified the role of damage-associated molecular patterns (DAMPs) and pattern recognition receptors (PRRs) in the development of NAFLD, leading to the activation of immune responses and inflammation. This review provides a comprehensive overview of the impact of DAMPs and PRRs on the pathogenesis of NAFLD.