The rise in obesity has led to increased metabolic diseases like insulin resistance, type 2 diabetes, and nonalcoholic fatty liver disease (NAFLD), the most common chronic liver disease globally. Factors like ethnicity, age, and lifestyle influence the risk of NAFLD. However, obesity significantly increases this risk, making individuals 3.5 times more likely to develop NAFLD and face higher risks for inflammation, fibrosis, and liver cancer. Understanding how immune-mediated inflammation drives NAFLD progression to NASH and liver cancer is key.
The liver’s immune system, including resident and recruited immune cells, plays a crucial role in managing metabolic liver diseases. Hepatocytes, macrophages, and liver sinusoidal endothelial cells (LSECs) regulate inflammation, while activated hepatic stellate cells (HSCs) drive fibrosis. Immune cells like Kupffer cells, T-cells, and macrophages contribute to liver inflammation and damage, promoting the transition from NAFLD to NASH and liver cancer. Continued research into this interaction may offer new treatment options.
Reference: Yahoo N, Dudek M, Knolle P, Heikenwälder M. Role of immune responses in the development of NAFLD-associated liver cancer and prospects for therapeutic modulation. J Hepatol. 2023 Aug;79(2):538-551. doi: 10.1016/j.jhep.2023.02.033. Epub 2023 Mar 7. PMID: 36893854.
