NEW DELHI: Inflammation alone may not be effective at combatting liver fibrosis in people with metabolic-associated fatty liver disease (MAFLD) as previously thought, finds a study, stressing the need for new measures to fight fibrosis or scarring of the liver.

MAFLD is a range of conditions caused by a build-up of fat in the liver.

Liver inflammation has long been considered a prerequisite to developing fibrosis, which can be explained as the scarring and thickening of tissue that can impair the liver's ability to function and lead to chronic liver disease and cancer.

But, reducing inflammation alone may not influence the extent of fibrosis, according to the study published in the Journal of Clinical Investigation.

Although inflammation is "still important, it may not be the main driver of fibrosis", said Tamer Sallam, associate professor at the University of California-Los Angeles (UCLA).

The team conducted a study in mice and focussed on a protein 'lipopolysaccharide-binding protein' (LBP), which is involved in the body's immune response.

The results showed that mice without LBP in their liver cells had lower levels of liver inflammation. While they had better liver function, no change was found in fibrosis.

In addition, the team also studied genetic analyses from large human datasets and human tissue samples from MAFLD patients at different stages of the disease.

They found that the LBP does not alter scar tissue markers.

Instead of just targeting inflammation, Sallam urged "more directed therapies" to better target fibrosis and improve the outcome.