Researchers at UCLA Health uncovered new information about the role inflammation plays in mitigating liver fibrosis, which is associated with metabolic-associated fatty liver disease (MAFLD), one of the most common diseases in the world affecting up to 40 percent of U.S. adults.
While inflammation in the liver has long been considered a prerequisite to developing liver fibrosis, the scarring and thickening of tissue that can impair the liver's ability to function, this new research suggests that reducing inflammation may not influence the extent of fibrosis. Liver fibrosis is the critical feature that creates chronic liver disease and liver cancer. If we can keep fibrosis in check then we can meaningfully impact liver disease.
Tamer Sallam, MD, Study Corresponding Author, Vice Chair and Associate Professor, Department of Medicine, David Geffen School of Medicine, University of California, Los Angeles He added, "For decades we have believed that targeting inflammation is one of the most important ways to reduce MAFLD. But this new research indicates that inflammation, while still important, may not be the main driver of fibrosis." The study, published in the Journal of Clinical Investigation, looked specifically at a protein called lipopolysaccharide binding protein (LBP), which is involved in the body's immune response, and how LBP functions in mice.
Findings showed that mice without LBP in their liver cells had lower levels of liver inflammation and better liver function but.