Liver fibrosis plays a critical role in chronic liver disease and liver cancer, affecting up to 40% of U.S. adults with MAFLD being a common disease.
Previous beliefs that targeting inflammation was crucial in reducing MAFLD are challenged by new research from UCLA Health indicating that reducing inflammation may not significantly impact fibrosis.
A study in the Journal of Clinical Investigation looked at the protein LBP and found that reducing inflammation through the absence of LBP in liver cells did not alter fibrosis levels in mice.
The research involved studying genetic data and tissue samples from MAFLD patients, confirming that LBP does not affect scar tissue markers.
The findings suggest that other pathways besides inflammation may be more effective in reducing fibrosis, pointing towards the need for more targeted therapies to improve outcomes for patients with liver diseases.
Researchers at UCLA Health have discovered new insights into the relationship between inflammation and liver fibrosis in individuals with metabolic-associated fatty liver disease (MAFLD), a common condition affecting a significant portion of the population. Liver fibrosis, which refers to the scarring and thickening of liver tissue, is a critical factor in the progression of chronic liver disease and liver cancer. While inflammation was previously thought to be a key contributor to fibrosis, the latest research suggests that reducing inflammation may not necessarily impact the extent of fibrosis.
The study, published in the Journal of Clinical Investigation, focused on a protein called lipopolysaccharide binding protein (LBP) and its role in the immune response within the liver. Findings from mouse models and genetic analyses of human datasets indicated that while reducing LBP levels led to decreased liver inflammation and improved function, it did not affect the development of fibrosis. These results challenge the long-held belief that targeting inflammation is the most effective strategy in managing MAFLD and suggest a need for further exploration into alternative therapies that could more effectively reduce fibrosis in patients.
Lead researcher Tamer Sallam emphasized the importance of finding ways to minimize scar tissue in the treatment of advanced liver diseases, noting that conventional methods of addressing inflammation may not be the most efficient approach. The study’s findings highlight the potential for more targeted therapies to address fibrosis and improve outcomes for individuals with MAFLD, paving the way for future research in this area.
