Scientists have discovered new insights regarding the role of inflammation in the reduction of liver fibrosis linked to metabolic-associated fatty liver disease (MAFLD), a prevalent condition impacting around 40% of adults in the United States.
Researchers at UCLA Health have revealed fresh information on how inflammation affects liver fibrosis related to metabolic-associated fatty liver disease (MAFLD), one of the most widespread illnesses globally, influencing nearly 40% of U.S. adults. Historically, liver inflammation has been viewed as a necessary factor in developing liver fibrosis, which involves the scarring and stiffening of liver tissue that can hinder its functionality. However, this recent study proposes that decreasing inflammation may not significantly change the level of fibrosis.
“Liver fibrosis is a key characteristic that leads to chronic liver disease and liver cancer. By managing fibrosis, we can greatly impact liver disease outcomes,” stated Tamer Sallam, MD, the lead author of the study and vice chair as well as associate professor in the department of medicine at the David Geffen School of Medicine at UCLA.
“For years, we have believed that addressing inflammation is one of the primary strategies to lessen MAFLD. However, this recent study shows that while inflammation remains important, it may not be the primary cause of fibrosis.”
The research, published in the Journal of Clinical Investigation, specifically examined a protein known as lipopolysaccharide binding protein (LBP), which plays a role in the immune response, and analyzed how LBP operates in mice. Results indicated that mice lacking LBP in their liver cells exhibited reduced liver inflammation and improved liver function, yet showed no alteration in fibrosis levels.
Besides animal models, the research team also evaluated genetic data from extensive human datasets and human tissue from MAFLD patients at various stages of the disease to explore the effects of diminished LBP function. The cumulative evidence suggested that LBP does not influence the markers of scar tissue.
Sallam emphasized the importance of further research into how LBP affects inflammation and whether alternative factors could lead to more effective inflammatory reductions and have a positive impact on reducing fibrosis.
“Minimizing scar tissue is one of the key goals in treating advanced liver diseases,” Sallam noted. “These findings imply that certain methods of addressing inflammation may not be effective, and that more focused therapies targeting different pathways could enhance our ability to manage fibrosis and improve patient outcomes.”
