Researchers at UCLA Health have found new information regarding the role of inflammation in mitigating liver fibrosis, a condition associated with metabolic-associated fatty liver disease (MAFLD), which affects up to 40 percent of U.S. adults. While it has long been believed that inflammation in the liver is necessary for the development of liver fibrosis, the study suggests that reducing inflammation may not have a significant impact on the extent of fibrosis. Liver fibrosis is a critical feature that leads to chronic liver disease and liver cancer, so understanding how to keep fibrosis in check could have a meaningful impact on liver health.
The study, published in the Journal of Clinical Investigation, focused on a protein called lipopolysaccharide binding protein (LBP), which is involved in the body’s immune response. Researchers found that mice without LBP in their liver cells had lower levels of liver inflammation and better liver function, but no change in fibrosis. The study also included genetic analyses from large human datasets and human tissue samples from MAFLD patients at different stages of the disease. Together, this evidence showed that the loss of LBP function does not alter scar tissue markers, indicating that targeting inflammation may not be the most effective way to reduce fibrosis.
Lead researcher, Tamer Sallam, emphasized the importance of finding more effective ways to target fibrosis in order to improve outcomes for patients with liver disease. While inflammation is still considered important in the development of MAFLD, the findings suggest that other pathways may offer more potent reductions in inflammation and have a greater impact on reducing fibrosis. Sallam highlighted the need for further research to better understand how LBP influences inflammation and to explore other potential therapies that could target fibrosis more effectively.
The discovery that reducing inflammation may not be the main driver of fibrosis challenges long-standing beliefs in the field of liver disease treatment. By studying both mouse models and human data, the researchers were able to gain a more comprehensive understanding of how LBP functions in liver health. The results suggest that targeting inflammation alone may not be sufficient to improve outcomes for patients with advanced liver diseases. Instead, more targeted therapies against other pathways may offer a more promising approach to reducing fibrosis and improving overall liver health.
The implications of these findings are significant for the treatment of MAFLD, a condition that affects a large portion of the population. By identifying new pathways that may be more effective in reducing fibrosis, researchers have opened up new possibilities for improving outcomes for patients with liver disease. Further research will be needed to confirm these results and to explore potential therapies that target fibrosis more directly. Ultimately, understanding the complex interactions between inflammation and fibrosis in the liver could lead to more effective treatments and better outcomes for patients with liver disease.