A new study suggests that focusing solely on inflammation may not be enough to tackle liver fibrosis in people with metabolic-associated fatty liver disease (MAFLD). This research highlights the need for new strategies to address liver fibrosis, which involves scarring of the liver.
MAFLD encompasses a range of conditions caused by fat accumulation in the liver. Traditionally, liver inflammation has been seen as a key factor in developing fibrosis, which can impair liver function and lead to chronic diseases and cancer.
However, the study published in the Journal of Clinical Investigation indicates that reducing inflammation alone might not impact the severity of fibrosis.
Tamer Sallam, an associate professor at the University of California-Los Angeles (UCLA), emphasized that while inflammation is still significant, it might not be the primary cause of fibrosis. The study, conducted in mice, focused on a protein called lipopolysaccharide-binding protein (LBP), which plays a role in the immune response.
The findings revealed that mice lacking LBP in their liver cells had reduced inflammation and better liver function. However, there was no change in the levels of liver fibrosis.
The research also analyzed genetic data from large human datasets and tissue samples from MAFLD patients at various disease stages. The results showed that LBP does not affect scar tissue markers.
Sallam recommended shifting focus from inflammation to more targeted therapies aimed directly at fibrosis. This approach could lead to better treatment outcomes for patients with MAFLD.
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